Everything she covered, taught rather than listed.

1.1 Intracranial Regulation and the Monro-Kellie Doctrine

Everything in this unit follows from one anatomical fact: the skull is a rigid, closed box. Inside it are exactly three things - brain tissue, blood (arterial, venous and capillary), and cerebrospinal fluid (CSF). Because the container cannot expand, the three contents are in permanent competition for a fixed volume.

Intracranial pressure (ICP) is the hydrostatic force measured in the brain's CSF compartment. Balance among the three components is what keeps it normal. Normal ICP is 5-15 mm Hg. A sustained pressure above 20 mm Hg is abnormal and the patient needs treatment. ICP can be measured in the ventricles, the subarachnoid space, the subdural space, the epidural space, or directly in brain tissue with a pressure transducer.

The Monro-Kellie doctrine

The doctrine states that the three components must stay at a relatively constant total volume inside the closed skull. If the volume of one component increases, volume from another must be displaced, and total intracranial volume - and therefore ICP - does not change. That displacement is compensation. It is limited. When the offending volume keeps growing, the other two components run out of room to give, compensation fails, and ICP climbs. Rising ICP compresses tissue, produces ischemia, and ends in cell death.

The three compensatory adaptations

• Change CSF volume - alter CSF absorption or production, or displace CSF down into the spinal subarachnoid space. This is the fastest and most usable buffer.
• Change intracranial blood volume - collapse of cerebral veins and dural sinuses, regional vasoconstriction or vasodilation, and changes in venous outflow.
• Change brain tissue volume - distention of the dura, or compression of brain tissue itself. This is the last and worst option, because compressing brain tissue is the injury you were trying to prevent.

What moves ICP even in a healthy person

Her slide lists six influences as bare words: arterial pressure, venous pressure, intraabdominal and intrathoracic pressure, posture, temperature, and blood gases - especially CO2. In the lecture she gave the mechanism behind three of them, and those mechanisms are what an application question tests.

1.2 Cerebral Blood Flow, Autoregulation, and CPP

Cerebral blood flow (CBF) is the amount of blood in milliliters passing through 100 g of brain tissue in one minute. Global CBF is about 50 mL/min/100 g. The brain has no fuel reserve, so it needs a constant supply: it consumes 20% of the body's oxygen and 25% of the body's glucose while weighing about two percent of the body.

Autoregulation

Cerebral autoregulation is the brain's automatic adjustment of the diameter of its own blood vessels to hold blood flow constant while systemic blood pressure moves around. Its purpose is to keep CBF consistent and to keep cerebral perfusion pressure within normal limits.

Autoregulation only works across a window of mean arterial pressure. It is effective when MAP is between 70 and 150 mm Hg. Below a MAP of 70, cerebral blood flow falls and symptoms of cerebral ischemia appear - she named syncope and blurred vision, where the slide says only "symptoms of cerebral ischemia." Above a MAP of 150, the vessels are already maximally constricted and have no further response to give; beyond that point, systemic pressure is transmitted straight into the head.

MAP itself is calculated as [SBP + 2(DBP)] / 3. She described it in plain language as "the pressure that keeps the arteries open, allowing sufficient blood flow to the organs and tissues," and gave a practical note: on higher-end monitors the number in parentheses next to the blood pressure is the MAP, so you rarely calculate it

by hand.

Cerebral perfusion pressure

Cerebral perfusion pressure (CPP) is the pressure needed to push blood through the brain. She drew the distinction cleanly: cerebral blood flow is the actual flow going to the cerebrum, and CPP is the pressure required to get that flow through. CPP is what ICP steals.

CPP = MAP - ICP. The relationship is the whole point of the unit: when ICP rises, CPP falls even if the blood pressure has not moved. That is why maintaining MAP matters so much in a patient with a high ICP, and why lowering ICP is a perfusion intervention rather than a number-chasing exercise. Cerebral vascular resistance - generated by the arterioles inside the cranium - links the two: CPP equals flow times resistance. She explained resistance by analogy to systemic vascular resistance: "what the cerebral arteries are pushing against to get blood flow adequately to the brain tissue."

What CO2 and oxygen do to cerebral vessels

Carbon dioxide, oxygen and hydrogen ion concentration all set cerebral vessel tone. Her framing for the CO2 half was "you may know CO2 is acidic, so anytime there's an increase in PaCO2 you're going to get dilation."

She defined cerebral oxygen tension as "the partial pressure of oxygen within the brain tissue - the level of oxygen that's available to the brain cells." If dilation fails to restore it, the tissue switches to anaerobic metabolism, lactic acid accumulates, and the environment turns acidic. Acidosis is itself a potent cerebral vasodilator, so the vessels dilate further in a continued attempt to increase flow. That is the point at which autoregulation is lost and compensatory mechanisms can no longer meet the tissue's metabolic demand. From then on, CBF is dictated directly by systemic blood pressure, hypoxia and catecholamines.

1.3 Increased ICP and Herniation

Increased ICP is a potentially life-threatening state resulting from an increase in any one - or all three - of the components inside the skull. It matters because it decreases CPP and therefore raises the risk of brain ischemia and infarction. The common causes are a mass - hematoma, contusion, abscess, tumor - and cerebral edema.

The cascade - the loop that makes ICP self-worsening

She narrated this entire cascade over a slide that carries no text at all, and it was one of her longest single explanations in the lecture. It is worth learning as a loop rather than a list, because the exam-relevant feature is that each step feeds the step before it.

• An insult to the brain produces tissue edema.
• Edema raises ICP.
• Rising ICP compresses the ventricles and the blood vessels.
• Compressed vessels mean decreased cerebral blood flow.
• Decreased flow means decreased oxygen delivery, and brain cells begin to die.
• Dead tissue draws more edema around the necrotic area - in her words, "once those brain cells die, you're going to get more edema around that necrotic tissue, and that more edema is going to increase the intracranial pressure even more."
• Higher ICP now compresses the brainstem and the respiratory center.
• Ventilation fails, so CO2 accumulates.
• CO2 causes vasodilation, which adds blood volume to a box that is already over-full - ICP rises again, and the loop closes on death.

Herniation

Herniation is brain tissue being forcibly shifted from an area of greater pressure to an area of less pressure. It converts a potentially reversible problem into an irreversible one, because the shift itself increases ischemia and edema. Herniation forces the cerebellum and brainstem downward through the foramen magnum - which she defined for the class, since the slide only names it: "the hole at the bottom of the skull that allows for the spinal cord to go through."

If the brainstem compression is not relieved, respiratory arrest follows, because the respiratory control center sits in the medulla. With continued herniation, brainstem death is imminent.

1.4 The Three Types of Cerebral Edema

Cerebral edema is an increased accumulation of fluid in the extravascular spaces of brain tissue. It raises tissue volume, and therefore raises ICP. The extent and severity of the original insult determine how much edema develops, and a single patient can have more than one type at once.

Symptoms of vasogenic edema, and the reporting rule

Vasogenic edema produces headache, decreasing consciousness progressing to coma, and focal neurologic deficits. The slide's warning is that headache can progress quickly to coma and death, so be vigilant. She turned that warning into an actual trigger phrase for calling the provider.

She also named what a focal neurologic deficit actually looks like, where the slide says only the phrase: "speech problems, poor coordination, motor control, changes in personality, or aphasia."

1.5 Manifestations of Increased ICP: Level of Consciousness

Her slide numbers the manifestations 1 through 6, and the order is not arbitrary - it runs roughly from earliest and most sensitive to latest and most ominous. Which manifestations appear depends on the cause of the pressure, its location, and how fast it is rising. A slow-growing tumor and an acute epidural bleed produce the same pressure by very different timelines.

A patient's state of consciousness is defined by clinical responses and by the pattern of brain activity recorded on an electroencephalogram (EEG). Changes can be dramatic - coma - or subtle: a flattening of affect, a change in orientation, a decrease in the level of attention. The subtle end is the dangerous end, because it is the end that gets charted as "patient seems tired."

Coma - the deepest state of unconsciousness

• No response to painful stimuli.
• Corneal and pupillary reflexes are absent.
• The patient cannot swallow or cough - which is the airway problem in section 1.14.
• Incontinent of urine and stool.
• EEG shows suppressed or absent neuronal activity.

1.6 Cushing's Triad and the Vital Sign Changes

Changes in vital signs are manifestation number two on her slide, and this is the single hardest-emphasized item in the entire module.

The abnormal breathing patterns behind "irregular respirations"

Her deck has two wordless slides of respiratory patterns. She narrated them briefly and pointed students to a video she posted on Canvas of Cheyne-Stokes breathing - a recommendation, not a requirement. The chapter supplies the table itself; it is reproduced here because "irregular respirations" is a category, not a finding.

These five come from Lewis, not from her slides. What she said about them is the practical instruction: note the respiratory pattern, not only the rate, because specific patterns are associated with severely increased ICP and each one localizes the injury a little lower in the brainstem.

1.7 Ocular Signs of Rising ICP

Manifestation number three. Four cranial nerves can be affected - CN II (optic), III (oculomotor), IV (trochlear) and VI (abducens) - but one of them carries almost all of the exam weight.

• Compression of CN III→ pupil dilation on the same side (ipsilateral) as the mass lesion, a sluggish or absent response to light, inability to move the eye upward and adduct, and ptosis of the eyelid.
• A fixed, unilateral, dilated pupil is a neurologic emergency indicating brain herniation.
• If ICP continues to rise, both pupils dilate - the first pupil enlarges until it is fully dilated, then the second follows.
• CN II, IV and VI problems produce blurred vision, diplopia, and changes in extraocular movements. These are three separate findings; blurred vision and diplopia are not the same thing.
• Central herniation→ sluggish but equal pupil response.
• Uncal herniation→ a dilated unilateral pupil.
• Papilledema - an edematous optic disc - is a nonspecific sign of persistent increased ICP.

How pupils are assessed and charted

• Compare pupils for size, shape, movement and reactivity.
• A normal reaction is brisk constriction when the light shines into the eye.
• The consensual response is slight constriction of the opposite pupil at the same time. This is on her slide; she did not say it aloud, so learn it from the deck.
• A sluggish reaction indicates early pressure on CN III - this is the one to catch.
• A fixed pupil with no response to light usually indicates increased ICP. The chapter adds other causes that must be ruled out: direct injury to CN III, previous eye surgery, atropine, and mydriatic eye drops.
• A hand-held pupillometer may be used to remove subjectivity - a chapter addition, not on her slides.

1.8 Motor Findings, Posturing, Headache, and Vomiting

Manifestations four, five and six. Motor change is the one with the localizing value; headache and vomiting are the ones students underweight because they sound benign.

Decrease in motor function

Contralateral hemiparesis or hemiplegia develops - on the side opposite the mass lesion. She isolated the vocabulary deliberately, because the slide uses both words as if they were interchangeable: hemiparesis is weakness or inability to move one side of the body; hemiplegia is partial or complete paralysis. Contralateral means opposite; ipsilateral means same side.

With painful stimuli the patient may localize - move toward the stimulus, which is the better response - or withdraw, moving away. Below withdrawal come the two posturing patterns, which occur because voluntary motor tracts from the cerebral cortex have been interrupted.

Headache

Headache in increased ICP comes from compression of intracranial structures. The chapter is precise about why: the brain itself has no pain receptors, so the pain is coming from arteries, veins and cranial nerves being squeezed. A nocturnal or early-morning headache is the concerning pattern - it suggests a tumor or another space-occupying lesion, because lying flat overnight raises ICP further. Straining, agitation or movement makes the pain worse, for the same venous-drainage reason from section 1.1.

Vomiting

Vomiting is a nonspecific sign of increased ICP related to the pressure change inside the cranium, and it may be projectile. The chapter adds a discriminator her slide omits: the vomiting of increased ICP is unexpected - not preceded by nausea. That is what separates it from gastrointestinal vomiting in a stem.

1.9 Complications: Inadequate Perfusion and the Herniation Syndromes

The two major complications of increased ICP are inadequate cerebral perfusion and cerebral herniation. Perfusion failure is section 1.2 arriving: as ICP climbs, CPP falls, and below 50 mm Hg neurons start dying. Herniation is the anatomical event.

Two structures decide where the tissue can go. The falx cerebri is a thin wall of dura folding down between the hemispheres, separating left from right. The tentorium cerebelli is a rigid fold of dura separating the cerebral hemispheres from the cerebellum - the chapter notes it is named for a tent, because it forms a tent-like cover over the cerebellum. Herniation syndromes are named for which of these edges the brain is pushed across.

1.10 Diagnostic Studies and Methods of ICP Monitoring

Diagnostic studies here are used to identify the cause of the increased pressure, not to confirm that pressure is high - the bedside assessment does that. Her list: CT and MRI, EEG, cerebral angiography, ICP measurement, PET, and brain tissue oxygenation measurement with a LICOX catheter.

Who gets an ICP monitor

• To guide care for any patient at risk for or with increased ICP.
• Patients with stroke, hemorrhage, tumor, infection, or traumatic brain injury.
• Patients with a Glasgow Coma Scale score of 8 or lessplus an abnormal CT or MRI. Both halves are required - the score alone is not the indication.
• The chapter adds that monitoring is done in the ICU, and is not used in patients with irreversible problems or advanced neurologic disease.

The three methods

Reading the waveform

ICP is displayed as a mean pressure in mm Hg, and the waveform has three components.

Inaccurate readings and infection

• Causes of inaccurate readings: a CSF leak around the monitoring device; obstruction of the catheter by blood clot or tissue; a difference in height between the catheter and the transducer; kinks in the tubing; incorrect height of the drainage system relative to the patient's reference point; bubbles or air in the tubing.
• Infection is the major complication of ICP monitoring. Contributing factors: monitoring for more than 5 days, use of a ventriculostomy, a CSF leak, and a concurrent systemic infection.
• Nursing: routinely assess the insertion site, use aseptic technique, and monitor CSF drainage for changes in color and clarity.

1.11 The Glasgow Coma Scale

The Glasgow Coma Scale assesses level of consciousness and, used serially, changing states. It scores three abilities: the ability to open the eyes to a verbal or painful stimulus, the ability to speak, and the ability to obey commands. The total is the sum of the three.

1.12 CSF Drainage and Cerebral Oxygenation Monitoring

If the patient has a ventriculostomy, you can control ICP by removing CSF. The provider writes the level at which to start draining and the frequency - intermittent or continuous.

Intermittent drainage - her worked example

"The doctor has an order that says, when the intracranial pressure is higher than 20, you need to drain. So what you'll do - you'll go to the system, you'll move the stopcock to allow for drainage, and you'll let it drain for about 2 to 3 minutes, and then close the stopcock again to make it a closed system." She also fixed the vocabulary in place: "when it's opened up, it's an open system; when it's closed, it's a closed system."

• Intermittent: the RN opens the system at the stopcock at the ordered ICP, drains for 2-3 minutes, then closes it again.
• Continuous: the drain stays open and you carefully monitor the amount of CSF drained - the risk here is taking off too much.
• Normal CSF production is 20-30 mL/hr, and total CSF volume is about 150 mL within the ventricles and subarachnoid space. Those two numbers are what make an hour of unwatched continuous drainage dangerous.
• Post a sign at the bedside so that anyone turning, suctioning or repositioning the patient knows it will affect drainage.
• The drain must be closed for 6 minutes before an ICP waveform reading is accurate. A number read off an open drain is not the patient's ICP.
• The chapter adds the complications her slide does not name: ventricular collapse, infection, and herniation or subdural hematoma formation from rapid decompression.

Cerebral oxygenation monitoring

Two separate technologies, measuring two different things. Her slide lists them together and it is easy to blur them; keep them apart.

1.13 Drug Therapy for Increased ICP

The goals of interprofessional care are to identify and treat the underlying cause - usually an increase in blood, brain tissue or CSF - and to support brain function by maintaining adequate oxygenation and preventing secondary injury. Early recognition and treatment produce better outcomes. Mechanical ventilation may be needed to keep PaCO2 in the normal range and maintain PaO2, and surgery may be needed if the cause is a mass.

1.14 Nursing Management of Increased ICP

Her four goals, in her order: (1) maintain a patent airway; (2) have ICP within normal limits; (3) have normal fluid, electrolyte and nutrition balance; (4) prevent complications from immobility and decreased level of consciousness.

Airway - the first goal for a reason

Maintaining the airway is a major nursing responsibility. As level of consciousness falls, the patient is at increased risk of obstruction. She gave the mechanism the slide implies: "their tongue can fall back and drop back into their throat, occluding their airway - and that's why a lot of these patients may need to be intubated or have some type of artificial airway." Increased secretions obstruct as well.

• Snoring sounds indicate obstruction and require immediate intervention. Not a comfort issue - a patency issue.
• Mechanical ventilation may be needed; monitor ABGs. The chapter adds the trigger: any patient with a GCS of 8 or less, or an altered LOC that prevents maintaining a patent airway or effective ventilation, needs intubation.
• Suctioning: keep it minimal and under 10 seconds.
• A nasogastric or orogastric tube prevents abdominal distention, which interferes with respiratory function - and, by the venous chain in section 1.1, raises ICP.
• The chapter adds two suctioning refinements her slides omit: give 100% oxygen before and after, and limit to 2 passes per procedure to avoid cumulative ICP rises.

Sedation

Pain, anxiety, fear and noxious stimuli all raise ICP, so sedatives, analgesics and paralytics are used. The difficulty is that these drugs alter the neurologic state and can mask the very changes you are watching for - which is why the pharmacology is chosen for short duration of action.

Fluid and electrolyte balance

Monitor IV fluids closely, track intake and output and daily weights, and follow serum electrolytes - especially glucose, sodium, potassium, magnesium and osmolality. Urine output is the parameter that detects the two opposite endocrine complications of brain injury. She reframed the reason: you monitor output not to prevent these so much as "to identify an issue like this that could be occurring."

Body position

• Keep the patient head up. Elevating the head of the bed promotes drainage from the head and decreases the vascular congestion that produces cerebral edema.
• Avoid extreme neck flexion - it obstructs venous outflow and raises ICP. Keep the head midline.
• Turn with slow, gentle movements. Rapid position changes raise ICP.
• Avoid pain and discomfort during turning, because pain raises ICP.
• Avoid extreme hip flexion - it raises intraabdominal pressure, which raises ICP.
• The chapter adds a limit her slides do not carry, and it is a good exam-level nuance: raising the head of the bed more than 30 degrees can decrease CPP by lowering systemic blood pressure. Higher is not automatically better; position for the best combination of ICP and CPP.
• The chapter also notes that turning, skin care and even passive range of motion can elicit posturing reflexes in some patients, and that patients are still turned at least every 2 hours to prevent atelectasis and contractures.

Protection from injury

• Agitation raises the risk of injury. Restraints may be needed, or a family member staying at the bedside. The chapter adds the caution that agitation may increase with restraints, which signals the need for a different approach.
• Seizure precautions: padded side rails, an Ambu bag at the bedside, readily available suction, accurate and timely administration of antiseizure drugs, and close observation.
• Antiseizure prophylaxis is recommended in severe brain injury. The chapter narrows this: prophylaxis is aimed at early seizures in the first 7 to 10 days, and is controversial for mild to moderate injury.
• She made the equipment concrete: "you might have seen in hospitals where they have those paddings on the side of the bed - so if a patient does have a seizure, they have something protecting them. And you want to have an Ambu bag at the bedside in case their respiratory function is declined."

Neurologic assessment techniques she demonstrated

1.15 Head Injury: Scalp Lacerations and Skull Fractures

She marked the transition plainly - "okay, so that was intracranial pressure" - and moved to head injury with about forty-four minutes left. Head injury means any injury to the scalp, skull, or brain. Traumatic brain injury (TBI) is the serious form. The most common causes are falls and motor vehicle accidents; others are firearms, assault, sports-related trauma, recreational injuries, and war-related injuries. The potential for poor outcomes is high.

Scalp lacerations

The easily recognized form of external head trauma. The scalp has many blood vessels with poor constrictive abilities, so profuse bleeding occurs even with relatively small lacerations. The complications are blood loss and infection.

Skull fractures

Skull fractures are described three ways: (1) linear or depressed; (2) simple, comminuted, or compound; (3) closed or open. Location determines the manifestations - the fracture line itself is less informative than what sits under it. The major complications are intracranial infection, hematoma, and meningeal and brain tissue damage.

Manifestations - reading the location off the face

Her slide names the classic findings: Battle sign, raccoon eyes, CSF rhinorrhea, tinnitus, deafness, loss of taste and visual changes. She located and defined them: Battle sign is "bruising behind the ear," raccoon eyes is "bruising around the eyes," and tinnitus is "ringing in the ears."

This location table is Lewis's, not hers - it is the Table 61.6 material she pointed students to. The one row worth learning cold is temporal, because it connects the fracture to the artery to the hematoma: a temporal fracture tears the middle meningeal artery, and that is how an epidural hematoma is made.

The CSF leak

Rhinorrhea is CSF leaking from the nose. Otorrhea is CSF leaking from the ear. Either one means the fracture has torn through the dura mater, which is why the leak matters far more than the volume of fluid suggests: there is now an open path between the outside world and the CSF.

1.16 Diffuse and Focal Brain Injury

The organizing split for brain trauma is whether the damage is spread out or localized.

Concussion

A minor diffuse head injury - a sudden, transient mechanical head injury with disruption of neural activity and a change in level of consciousness. The classic signs are a brief disruption in LOC, retrograde amnesia about the event, and headache. It resolves spontaneously and is usually considered benign.

Postconcussion syndrome develops 2 weeks to 2 months after the injury in some patients: persistent headache, lethargy, personality or behavior changes, a shortened attention span, decreased short-term memory, and changes in intellectual ability.

Diffuse axonal injury

Her slide lists "axonal injury" as two words. She defined it and gave two mechanisms: "axonal injury is when the brain's nerve fibres tear - the brain can shift or rotate in the skull. So this can happen with a car crash, or like shaken baby syndrome."

The chapter fills in what her slide and lecture leave out, and it contains the timing fact most likely to be tested: axonal damage is not an immediate tearing. Trauma changes the function of the axon, which then swells and disconnects, and that process takes 12 to 24 hours to develop and may persist longer. Clinically it produces decreased LOC, increased ICP, decortication or decerebration, and global cerebral edema. Severe DAI carries a poor functional prognosis, and survivors go to the ICU to be watched for rising ICP.

Lacerations of brain tissue

A focal injury involving actual tearing of brain tissue, occurring with depressed and open fractures and penetrating injuries. Management is antibiotics until meningitis is ruled out and preventing secondary injury from increased ICP. If bleeding is deep within brain tissue, both focal and generalized signs develop. The chapter adds the blunt reason there is no surgical option: surgical repair of a brain laceration is impossible because of the nature of brain tissue.

In major head trauma, delayed responses occur - bleeding, hematoma formation, seizures, cerebral edema. Subarachnoid and intraventricular hemorrhage can both result from head trauma. Intracerebral hemorrhage is generally due to a cerebral laceration and behaves as a space-occupying lesion: unconsciousness, hemiplegia on the contralateral side, and a dilated pupil on the ipsilateral side - the localizing pair from section 1.7.

Contusion

A bruising of brain tissue within a focal area, associated with closed head injury and often occurring at a fracture site. There may be areas of bleeding, infarction, necrosis and edema. Overall prognosis is based on the amount of bleeding around the contusion site.

Contusions may continue to bleed or rebleed. The chapter's word for this is that they "blossom" on subsequent CT scans, and that bleeding worsens the neurologic outcome. Neurologic assessment may show focal or generalized manifestations depending on size and location. Seizures occur especially with frontal or temporal lobe involvement. And anticoagulant use and coagulopathy are associated with increased bleeding, more severe injury, and increased mortality - her slide flags this as very important in older adults.

Emergency management and diagnostics

• If unresponsive, assess circulation, airway, breathing. If responsive, monitor airway, breathing and circulation.
• Assume a neck injury with every head injury - stabilize the cervical spine.
• Apply oxygen by nonrebreather if needed.
• Establish IV access with two large-bore catheters. The chapter specifies the fluid: normal saline or lactated Ringer's.
• Intubate if the GCS is below 8.
• Control external bleeding with a sterile pressure dressing.
• CT scan is the primary study. MRI is more sensitive than CT for small lesions. Transcranial Doppler measures CBF velocity - she added that it "shows the speed and direction of blood flow, and any presence of blood clots as well."
• The chapter adds a caution for ongoing care: give fluids cautiously, because fluid overload raises ICP.

1.17 The Three Hematomas

She defined the word first, because the slide assumes it: "a hematoma is pretty much like a large bruise underneath the skin, or a collection of blood underneath the skin - and in this case, in the brain." The three are named for where the blood collects relative to the dura.

Subdural hematoma by timing

• Acute subdural manifestations: decreasing LOC, headache, drowsiness, confusion, unconsciousness, and ipsilateral pupil dilation and fixation if the ICP is significantly increased.
• Chronic subdural manifestations: the presenting problem is focal symptoms rather than signs of increased ICP. The chapter gives the reason: brain atrophy in older adults creates a larger subdural space, so a hematoma has room to grow without pushing pressure up - and the same atrophy puts bridging veins under tension, making them easier to tear.
• The chapter adds that a history of alcohol use raises the risk, because of falls.

1.18 Cranial Surgery

She deliberately front-loaded burr holes so that the next slide would make sense - "I want to talk about [burr holes] before we talk about this, because burr holes are included in these procedures." That is the right order to learn them in, because a burr hole is the building block of everything else.

Stereotactic procedures

A stereotactic biopsy obtains tissue samples for histologic examination. The surgeon drills a burr hole or creates a bone flap for the entry site, then introduces a probe and a biopsy needle. She gave the indication in patient terms: "if a patient has a tumor, or something that needs to be tested to see if these are benign or malignant cells." Other stereotactic procedures remove small brain tumors and abscesses, drain hematomas, perform ablative procedures for diseases such as Parkinson's, and repair arteriovenous malformations. The major advantage is reduced damage to surrounding tissue.

Stereotactic radiosurgery targets tumor cells and other abnormal growths. She made the point the slide does not say outright - it is radiation, not surgery: "the stereotactic radiosurgery is just going to be like a radiation procedure to target those tumor cells, if a patient does have a malignant brain tumor." The chapter agrees and adds the hardware: a linear accelerator, Gamma Knife or CyberKnife, with the head held still in a stereotactic frame, delivered in one session of a few hours or in several sessions.

Ongoing nursing management after head injury

• Monitor for increased ICP - every head-injury patient is at risk.
• Assess the GCS, neurologic status, and whether a CSF leak has occurred.
• Use a calm, gentle approach. She gave the reasoning: "they might be scared - what's going on? And if they have increased intracranial pressure, you also don't want to increase that even more by putting them in a stressful environment."
• Report any change in neurologic state, even if subtle.
• Her goals for the patient with acute head injury: maintain adequate cerebral oxygenation and perfusion; stay afebrile; be free of discomfort; be free from infection; have adequate nutrition; attain maximal cognitive, motor and sensory function.

2.1 How the Kidneys Work, and What Acute Kidney Injury Is

She opens with normal physiology and says why: "it's always helpful with, uh, you know, when you're doing any kind of system or any issues with a system to go back and just look at how the system should be working." Her slide is a six-box flow diagram, and the boxes are the spine of what follows - each of the three causes of AKI is a failure at one of these steps.

Blood enters through the renal arteries, which branch into arterioles; arterioles reach a nephron and form the glomerulus, whose fenestrations let certain products through and keep others out. Blood is filtered at the glomeruli, tubular reabsorption puts some of the filtrate back into the blood, and what is left becomes urine, carried down the ureters to the bladder and out through the urethra. Cleaned blood leaves by the renal vein.

Acute kidney injury

AKI is a rapid loss of kidney function, with or without decreased urine output. Note the second half of that sentence - output can be normal and the kidneys can still be failing. It is accompanied by rising blood urea nitrogen (BUN), creatinine (Cr) and potassium, and severity runs from a small rise in creatinine to frank azotemia, the accumulation of nitrogenous waste products in the blood. AKI develops over hours to days and is potentially reversible. Its causes are prerenal, intrarenal and postrenal.

Her slide prints BUN at 6-24 mg/dL and creatinine at 0.7-1.3 mg/dL (males), 0.6-1.1 mg/dL (females), with no explanation. She defined both analytes from scratch: urea is "a waste product that your body creates, uh, when it breaks down protein," and creatinine is "a waste product that comes from breakdown of muscle tissue and protein in food." Those two definitions are why creatinine turns out to be the better marker in section 2.6.

2.2 Causes of AKI: Prerenal and Intrarenal

Prerenal

Prerenal causes reduce systemic circulation, so renal blood flow falls, and less flow means less glomerular perfusion and less filtration. Nothing is wrong with the kidney tissue; the kidney is being starved from upstream. Autoregulation fires to protect essential organs, and she walked the chain where the slide only lists hormones: angiotensin II "increases blood pressure and it stimulates the release of aldosterone, and then aldosterone increases sodium and water retention," with ADH and norepinephrine doing the same work by other routes. The result is prerenal azotemia - decreased sodium excretion, increased sodium and water retention, decreased urine output.

Compensation does not last. She generalised the failure point herself: "like like we always say, with any, um, uh, regulatory mechanism or compensatory mechanism, it eventually does fail." When decreased perfusion persists, the compensatory mechanisms give out and the prerenal problem becomes an intrarenal one. A prerenal cause left alone long enough stops being prerenal.

Intrarenal

Intrarenal causes damage kidney tissue directly, impairing nephron function. Her four sources are prolonged ischemia, nephrotoxins, hemoglobin from hemolysed red cells and myoglobin from necrotic muscle. She stopped on the nephron image to call it "one of the most important areas of the kidney" - one of only two things in the lecture she called most important - and supplied the mechanism the slide omits: nephrotoxins damage tubular epithelial cells or crystallise and obstruct intrarenal structures, and the obstruction provokes inflammation. Myoglobin behaves the same way, since "high levels of myoglobin can precipitate in the renal tubules, also causing more obstruction and direct kidney damage." Lewis adds that both pigments also cause renal vasoconstriction.

Acute tubular necrosis

ATN is the most common intrarenal cause of AKI in hospitalised patients. Severe ischemia disrupts the basement membrane and destroys tubular epithelium in patches; nephrotoxins necrose tubular epithelial cells, which slough off and plug the tubules. It follows ischemia, nephrotoxins or sepsis, and ischemic and nephrotoxic causes account for 90% of intrarenal AKI. Her other in-hospital risk factors are major surgery, shock, blood transfusion reaction, muscle injury from trauma, and prolonged hypotension. ATN is potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates - one conditional, and it is why that structure is worth knowing by name. Note that Lewis states the claim two ways: Table 51.1 (p.1233) gives the most common cause of AKI, full stop, as ATN, while the body text (p.1234) scopes it to the most common intrarenal cause in hospitalised patients. Her slide follows the narrow version and so does this guide, because it survives a question that also offers a prerenal option.

2.3 Causes of AKI: Postrenal

This was her third-longest stop - 467 words, about 2.9 minutes - on the category Lewis says causes fewer than one AKI case in ten, and she spent it on mechanism rather than on the list. Postrenal causes involve mechanical obstruction to the outflow of urine. Urine refluxes into the renal pelvis, pressure inside the kidney rises, kidney structures are damaged, and filtration falls. Her common causes are BPH, prostate cancer, stones, trauma and external tumors. She self-corrected the anatomy mid-sentence here - obstruction "is going to prevent, uh, urine flow of down the urethra. Uh, sorry. The ureters. Ureters, as it should be" - and she had been pointing at the next slide's figure since two slides earlier, promising "I have a picture which I'll show you after, actually." Bilateral ureteral obstruction produces hydronephrosis - dilation of the kidney - with raised hydrostatic pressure and tubular blockage behind it.

2.4 The Clinical Course of AKI and the RIFLE Classification

Prerenal and postrenal AKI usually resolve quickly with treatment, provided they have not already caused intrarenal damage. Once intrarenal damage occurs, AKI runs a prolonged course through three phases - oliguric, diuretic, recovery. Lewis adds the outcome she leaves implicit: when a patient does not recover from AKI, CKD may develop.

RIFLE is the classification her deck and Lewis both use to stage AKI, and it is the only one either contains. There is no KDIGO staging in this deck, in this lecture, or in the AKI half of Ch. 51 - a search returns nothing in any of the three. If you have met KDIGO stages 1-3 elsewhere, they are not what this material uses. The letters are three stages of severity - Risk, Injury, Failure - followed by two outcome variables, Loss and

End-stage renal disease. Each of the first three is met by either the creatinine criterion or the GFR criterion or the urine output criterion. Read the table as a pattern rather than a list of numbers: the creatinine multiples run 1.5, 2, 3 and the GFR losses run 25%, 50%, 75%, moving together at every stage; the urine output threshold falls only once, at Failure, while what changes at Risk and Injury is the duration - 6, then 12, then 24 hours. Loss and ESRD are measured not in creatinine but in time.

2.5 The Oliguric Phase: Urine, Fluid Volume, Acid-Base, and Sodium

Slide 13 is the longest single stop in the lecture - 745 words, about 4.7 minutes, 2.9 times her average - and roughly a third of it is off-slide. She interrupted herself before starting the phase at all: "Oh, and here, let me just clarify a couple definitions."

Urinary changes

Oliguria is a urine output of less than 400 mL in 24 hours. It usually appears within 1 to 7 days of the injury, and within 24 hours if the cause is ischemia. The phase lasts 10 to 14 days on average and can run months, and the longer it lasts the poorer the prognosis for complete recovery. The pattern points at the cause: oliguria usually accompanies prerenal causes, anuria usually accompanies postrenal obstruction, and nonoliguric AKI - an output above 400 mL/24 hr, in about 50% of patients - accompanies the intrarenal causes, acute interstitial nephritis and ATN.

Urinalysis may show casts, RBCs and WBCs - Lewis explains what the casts are, where her slide only names them: mucoprotein impressions of necrotic tubular epithelial cells sloughed into the tubules. Specific gravity fixes at around 1.010 and urine osmolality at about 300 mOsm/kg, both of which are the values of plasma. Proteinuria may be present if the AKI involves glomerular membrane dysfunction, and her reasoning generalises to every proteinuria question in this unit: "proteins are large molecules and they should not be making it through that filtration process."

Fluid volume, acid-base and sodium

Hypovolemia can worsen all forms of AKI. Falling urine output produces fluid retention, and severity tracks the amount held: distended neck veins with a bounding pulse, edema and hypertension first, then heart failure, pulmonary edema, and pericardial and pleural effusions.

The damaged kidney cannot excrete hydrogen ions, so acid accumulates. She explained the bicarbonate half twice over, because two things happen to it at once: production falls, since reabsorption and regeneration of HCO3 are defective, and the existing supply is spent - "we're using the one that's already the bicarb, that's already present" - buffering the acid already there. Severe acidosis produces rapid, deep respirations to blow off CO2.

Damaged tubules cannot conserve sodium, so urinary sodium excretion rises and serum sodium ends up normal or low. Excess sodium intake is avoided because it drives volume expansion, hypertension and heart failure - and she gave the mechanism the slide leaves out, "when there's sodium, uh, there's also going to be water that's following it." Uncontrolled hyponatremia may lead to cerebral edema, because low serum sodium moves water into brain cells and swells them.

2.6 The Oliguric Phase: Potassium, and the ECG Changes She Never Named

Potassium is the most repeated topic in the recording: the word appears 53 times and "hyperkalemia" 27 times across 12 different slides, the only subject she returns to on more than ten. Two of her nine "very important" flags land eight lines apart on this one slide.

The kidneys normally excrete 80% to 90% of the body's potassium. In AKI they cannot secrete it, so serum potassium rises, and her slide adds three further sources - each a different route to the same number.

• Trauma. Damaged cells release potassium as they break open, on top of what the kidney is failing to clear.
• Bleeding and blood transfusions. Cellular destruction releases potassium into the extracellular fluid.
• Metabolic acidosis. Hydrogen ions move into cells and potassium is driven out into the ECF - and she gave the reason the slide does not, "because both potassium and hydrogen are positively charged."

What hyperkalemia does to the heart

Her slide says hyperkalemia is often asymptomatic, that the patient is weak with severe hyperkalemia, that there are ECG changes, and that cardiac muscle is intolerant of acute rises in potassium, so emergency treatment is needed - a bullet she did not read. What she gave instead is a mechanism on no slide: high potassium disrupts "the electrical stability of the heart by, um, altering the resting membrane potential. This leads to impaired conduction, decreased excitability," and from there "potentially leading to life threatening arrhythmias or cardiac arrest."

The morphology comes from Lewis's Ch. 17, the assigned re-read, which sequences it rather than listing it (p.314): "The initial finding is tall, peaked T waves. As potassium increases, cardiac depolarization decreases. This leads to loss of P waves, a prolonged PR interval, ST segment depression, and widening QRS complex. Life-threatening dysrhythmias may occur." Read in that order, the three items on her slide are the first, fourth and fifth events in one progression, and the two she does not print - loss of P waves and a prolonged PR interval - fall between them.

Hematologic, waste and neurologic problems

Leukocytosis occurs, and her slide states flatly that the most common cause of death in AKI is infection - though eleven slides later she pulled back mid-sentence on it, "infections are the leading cause of, uh, death in patients with, um. Oh, one of the leading complications." Her slide and Lewis's Table 51.1 both say cause of death. BUN and creatinine both rise, but creatinine is the best serum indicator in AKI - and she gave the reason, which is not on the slide: BUN "can be affected by other things such as dehydration, steroids, um, severe injury or GI bleeding." Creatinine is better because it is not moved by those things. Neurologic changes appear as nitrogenous wastes accumulate in the brain and nervous tissue, escalating from mild to seizures and coma.

2.7 The Diuretic Phase, the Recovery Phase, and Diagnosing AKI

In the diuretic phase daily urine output is usually 1 to 3 litres and can reach 5 or more, and the phase lasts 1 to 3 weeks. The trap is that the volume looks like recovery and is not: the nephrons are still not fully functional. What has returned is the ability to excrete wastes; what has not is the ability to concentrate urine. On top of that, the high BUN in the filtrate causes osmotic diuresis, dragging water out with it.

The recovery phase begins when GFR increases, letting BUN and creatinine fall. She also defined GFR here, in passing, for a term the deck uses from slide 12 onward and never explains - it "pretty much tells you how much blood is being filtered out from the kidneys within a, uh, within a minute." Major improvements occur in the first 1 to 2 weeks, but it may take 12 months for kidney function to stabilise. Some patients never recover and progress to end-stage renal disease; Lewis adds that those who do recover may reach clinically normal function and still sit in an early stage of CKD.

Diagnostic studies

The history is essential for identifying which cause is operating, and Lewis makes the mapping explicit where her slide only says "history is essential": suspect prerenal with dehydration, hypotension or blood loss; intrarenal after nephrotoxic drugs or contrast; postrenal with changes in the urinary stream, stones, BPH, or bladder or prostate cancer. Urine output and serum creatinine occur late and are lagging indicators: a rise in creatinine may not appear until more than 50% of kidney function is lost, and the rate of rise determines severity, not the single value. Urinalysis showing casts, protein and abundant cells indicates intrarenal AKI, as do hematuria, pyuria and crystals.

• Renal biopsy is the best way to confirm an intrarenal cause - confirmatory, not first-line.
• Kidney ultrasound is often the first test done, because it images without exposing the patient to nephrotoxic contrast. It assesses kidney blood flow, tubular function and the collecting system, and evaluates obstruction.
• CT shows lesions, masses, obstruction and vascular abnormalities; she added that non-contrast CT is acceptable for stones in a patient who already has AKI.
• MRI or MRA with gadolinium contrast can be potentially fatal and is not advised.

2.8 Managing AKI: Interprofessional Care, Nursing Care, and Prevention

The goals are to eliminate the cause, manage the signs and symptoms, and prevent complications while the kidneys recover. Nothing here repairs a nephron; all of it buys time.

Fluid restriction and diuretics

Fluid intake is restricted in the oliguric phase, and her slide gives the arithmetic: add all losses for the previous 24 hours - urine, diarrhea, emesis, blood - and add 600 mL for insensible losses from respiration and diaphoresis. That total is the next day's allowance - and she spent much of this 480-word slide not on the formula but on where its numbers come from, "charted in your computer system... So the previous nurse should have been, uh, should be charting and then you should be charting." The calculation is only as good as the previous shift's intake and output record. Loop diuretics (furosemide) and osmotic diuretics (mannitol) are then used to manage overload, with the goal of increasing urine output and maintaining a nonoliguric state, which may help protect the kidneys. Her slide states the double-edge in the same breath: diuretics can also cause further fluid depletion and decrease renal blood flow, worsening the AKI.

Treating hyperkalemia

Hyperkalemia is one of the most serious complications of AKI and has to be treated. Slide 23 was her second-longest stop at 552 words. Her four measures do three different jobs, and she was sharper about the distinction than the slide is.

Renal replacement therapy and nutrition

Conservative therapy may be all that is needed until kidney function improves. When it is not, her indications for RRT are volume overload compromising cardiac or pulmonary status, high serum potassium, metabolic acidosis, BUN over 120 mg/dL, significant mental status change, pericarditis, pericardial effusion, or cardiac tamponade - and she sharpened that mental status item to "a very severe change." The modalities are HD, PD and CRRT. On nutrition: adequate calories to prevent catabolism and adequate protein, energy mainly from carbohydrate and fat to prevent ketosis, sodium restricted, and enteral nutrition preferred when oral intake fails - with the numbers her slide omits supplied by Lewis, 30 to 35 kcal/kg and 0.8 to 1.0 g protein/kg of desired body weight.

Nursing assessment

Daily weights, with the rationale she added - "checking at the same time each day on the same scale to get the most accuracy" - and 1 kg equals 1000 mL of fluid. Strict intake and output, vital signs, and urine assessment for colour, specific gravity, glucose, protein, blood and sediment. Edema, neck vein distention, bruises; the dialysis access site for inflammation or exudate; mental status; lungs for crackles, wheezes or decreased breath sounds; ECG monitoring. Lewis adds the oral mucosa, and listening for an S3 gallop, murmur or pericardial friction rub. Her clinical problems for AKI are electrolyte and fluid imbalance, risk for infection, and anxiety.

Prevention

Prevention and recognition of AKI are the most important aspects of care, and the centrepiece is contrast-induced nephropathy (CIN) - nephrotoxic injury from contrast media given for diagnostic studies.

• Ensure adequate fluid intake if contrast is given to a high-risk patient - she added the order that accompanies it, "most of the times when a CT with contrast is ordered, I.V. fluids are ordered alongside with it." Lewis adds that the best way to avoid CIN is to avoid contrast, using ultrasound instead.
• Hold metformin for 48 hours before and after contrast to reduce the risk of lactic acidosis, and monitor kidney function in anyone on potentially nephrotoxic drugs, given in the smallest effective dose for the shortest period (Lewis).
• Caution patients about OTC drugs that worsen kidney function, especially NSAIDs - she named "ibuprofen, Aleve."
• ACE inhibitors can decrease perfusion pressure and cause hyperkalemia, and may have to be stopped if it cannot be controlled - yet they are also used to prevent proteinuria and slow progression, especially in diabetes. She named a dose the deck does not, "a really small dose like 2.5 mg of lisinopril," and said the logic is hard: "it's kind of an interesting and kind of confusing at the same time."

Infection, teaching and older adults

Use aseptic technique. Patients with AKI have a blunted febrile response, so they may not have a fever - look for local signs and leukocytosis rather than waiting on a temperature. Antibiotic type, dose and frequency need careful consideration, because the kidneys are the main route of excretion for many antibiotics. Teach the signs of recurrent kidney disease and provide psychosocial care. Older adults are at increased risk because GFR declines with age; Lewis adds that the aging kidney compensates poorly for changes in fluid volume, solute load and cardiac output, and that patients over 65 are less likely to recover - though age is not a barrier to offering RRT, a point she makes herself on slide 56.

2.9 Her Two AKI Application Slides, Worked from the Chapter

Slides 28 and 29 close the AKI half with application questions. She spoke to neither - not a word on either slide - going straight from "So to be aware with that with elderly patients" into "Okay, so that was acute kidney disease." Her disposition for the whole deck was her closing line: "All right, that's it. So I'll go ahead and upload this and then we'll go over it in class." Her answers are therefore not on the recording at all. What follows is worked from Lewis's Ch. 51, and none of it should be read as her reasoning.

Slide 28 - "What is the cause of AKI in a patient who..."

Slide 29 - priority nursing interventions in the diuretic phase

Ch. 51's diuretic-phase text and its AKI Nursing Management section together give the priorities for the fluid reversal described in section 2.7.

• Monitor for hypovolemia and hypotension - Ch. 51: "Hypovolemia and hypotension can occur from massive fluid losses." The phase's characteristic danger, and the reverse of the oliguric phase's.
• Monitor and replace fluid and electrolytes. Ch. 51 names three risks - hyponatremia, hypokalemia and dehydration. Potassium has reversed direction.
• Strict intake and output, and daily weights on the same scale at the same time; 1 kg equals 1000 mL. Ch. 51 makes the nurse's role in fluid and electrolyte balance explicit "during the oliguric and diuretic phases."
• Watch laboratory values for stabilisation, since those values levelling off near the end of this phase is how you know recovery is starting.
• Continue infection precautions and avoid nephrotoxins. Infection remains the leading cause of death in AKI, the febrile response is still blunted, and the nephrons are not fully functional however reassuring the output looks.

2.10 Chronic Kidney Disease: The Disease, and How Kidney Function Is Measured

CKD is a progressive, irreversible loss of kidney function, and it is more common than AKI. Her risk factors are aging, obesity, diabetes, hypertension, family history of CKD, and exposure to nephrotoxic drugs. Two facts on her banner slide explain why it is diagnosed late: the kidneys are highly adaptive, so CKD may not be recognised until considerable nephron loss has happened, and 70% of people with CKD are unaware they have it. Lewis adds the leading causes her slide omits - diabetes at about 50%, hypertension at about 25%.

Manifestations come from retained urea, creatinine, phenols, hormones, electrolytes and water.Uremia is the syndrome in which kidney function has declined to the point that symptoms appear in multiple body systems, usually at a GFR of 15 mL/min or less. In early CKD there are usually no urine changes; as it progresses, fluid retention appears, which she translated to the bedside - "if a patient comes in like leg swelling or difficulty breathing." As GFR falls, BUN and serum creatinine rise, but creatinine clearance, the estimated GFR, is a more accurate indicator of kidney function than BUN or creatinine in CKD. A rising BUN itself produces nausea, vomiting, lethargy, fatigue, impaired cognition and headaches.

2.11 CKD Manifestations, System by System

Slides 33 through 38 walk the body, and her time across them is uneven in a way worth noticing: 428 words on the metabolic and potassium slide, 205 on the neurologic slide, which is one of the densest in the deck.

Carbohydrate metabolism, triglycerides and potassium

Her slide reads "hyperglycemia and hyperinsulinemia may occur", with insulin depending on the kidneys for excretion so that it stays in the circulation longer in CKD; what she taught from that bullet was the opposite word and a more usable point. Hyperinsulinemia drives hepatic triglyceride production, and most patients with CKD die from cardiovascular disease. On potassium, fatal dysrhythmias can occur when serum K+ reaches 7-8 mEq/L, and the causes in CKD are reduced renal excretion, breakdown of cellular protein, bleeding and metabolic acidosis, with more arriving from foods, supplements, drugs and IV infusions.

Sodium, magnesium and acid-base

Sodium may be high, low or normal. Impaired excretion causes sodium and water retention, and retaining large volumes of water produces dilutional hyponatremia - the serum sodium reads low because it has been diluted, not because sodium was lost. The consequences are edema, hypertension and heart failure. Hypermagnesemia occurs if the patient ingests large amounts of magnesium, which she called "very rare" and tied to the antacid and laxative teaching; its manifestations are absent reflexes, decreased mental status, dysrhythmias and hypotension. Metabolic acidosis arises exactly as in AKI.

Anemia, bleeding and infection

Anemia is due to decreased erythropoietin production, since erythropoietin is made in the kidneys and normally stimulates precursor cells in the bone marrow to make red cells. Contributors are nutritional deficiencies, decreased RBC life span, increased hemolysis, frequent blood draws and GI bleeding, and increased PTH inhibits erythropoiesis and shortens RBC survival; patients on dialysis may need IV iron plus folic acid. A defect in platelet function produces bleeding tendencies, and infection risk rises from altered WBC function and immune response.

Cardiovascular, respiratory and gastrointestinal

The most common cause of death in CKD is cardiovascular disease, related to vascular calcification and arterial stiffness - which she attributed partly to "accumulation of toxins in the bloodstream um which restrict blood flow" plus "microvascular damage... which impairs the ability to dilate and deliver blood flow." Hypertension is worsened by sodium retention and increased extracellular fluid volume, which is why blood pressure control is one of the most important therapeutic goals in CKD management - one of only two things in 136 minutes she called most important. Dysrhythmias follow hyperkalemia and decreased coronary perfusion, and uremic pericarditis can progress to pericardial effusion and cardiac tamponade.

Respiratory findings are Kussmaul breathing in severe acidosis and dyspnea from fluid overload, pulmonary edema, uremic pleuritis, effusion and infection. The GI list is stomatitis, metallic taste, periodontal disease, uremic fetor, anorexia, nausea and vomiting, weight loss, GI bleeding and constipation. She explained two of those: uremic fetor is urea in the saliva broken down by mouth bacteria into ammonia - "it's pretty bad. It smells like urine" - and stomatitis is urea irritating the oral mucosa. Both are why mouth care is a nursing intervention in kidney failure rather than a comfort measure.

Neurologic

Neurologic change comes from increased nitrogenous waste, electrolyte imbalance, metabolic acidosis, and atrophy and demyelination of nerve fibres. Early: lethargy, apathy, decreased concentration, fatigue, irritability. Later: seizures and coma from rapidly rising BUN and hypertensive encephalopathy. Dialysis should improve or halt CNS problems.Altered mental status is a late manifestation and rarely occurs unless the patient has chosen no treatment.Peripheral neuropathy slows nerve conduction to the extremities, producing paresthesias in the feet and legs as a burning sensation, and with motor involvement bilateral foot drop, muscle weakness and loss of deep tendon reflexes, plus night-time leg cramps and asterixis.

2.12 CKD Mineral and Bone Disease

Slide 39 was her fourth-longest stop at 538 words, about 3.4 minutes, and it is one cascade rather than a list. CKD-MBD is a systemic disorder of mineral and bone metabolism caused by progressive deterioration of kidney function. Learn it as a chain, because every treatment in section 2.15 breaks one of its links.

• Less vitamin D is converted to its active form, because activation is a kidney function.
• Serum vitamin D falls, and with it serum calcium - active vitamin D is what lets calcium be absorbed.
• Hypocalcemia stimulates increased secretion of parathyroid hormone (PTH), which is secreted by the parathyroid glands.
• PTH stimulates bone demineralisation, releasing calcium and phosphate out of bone to raise the serum calcium.
• That release raises serum phosphate, on top of the hyperphosphatemia already produced by decreased phosphate excretion, and leaves the patient at high risk of fractures from increased bone remodelling.

She taught this whole loop four slides early, on the anemia slide, before the deck reached it: "kidneys are usually supposed to activate vitamin D properly... since this vitamin D is not being activated, the parathyroid glands are triggered to produce more parathyroid hormone so that the body can attempt to raise calcium levels." That early version is the clearest one she gave, and it is where the PTH-inhibits-erythropoiesis line on the anemia slide comes from.

• Osteomalacia - bones soften and deform, because demineralised bone has lost the mineral that made it rigid.
• Osteitis fibrosa - decalcification, with bone tissue replaced by fibrous tissue, as sustained high PTH keeps resorbing bone.
• Vascular calcification - calcium and phosphate deposits in vessel walls, her mechanism rather than the slide's. What was pulled out of bone has to go somewhere, and this is a significant contributor to CVD.
• Cardiac calcification - deposits in heart tissue, "particularly coronary arteries" in her addition, which can disrupt the conduction system and cause cardiac arrest.

The gold standard for diagnosing CKD-MBD is bone biopsy - printed in capitals on her slide, and the only gold standard named anywhere in this deck.

2.13 CKD: Skin, Reproduction, Mood, and the Whole-Body Picture

Itching comes from three sources her slide names together - dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy - and the middle one is a direct consequence of section 2.12. Uremic frost is a rare condition in which urea crystallises on the skin, seen only when BUN is above 200 mg/dL. Reproductive effects are infertility and decreased libido, menstrual changes including amenorrhea and anovulation, and decreased testosterone with low sperm counts. Her last line is simply psychologic changes.

2.14 CKD Diagnostic Studies and the Five Stages

Persistent proteinuria is the first sign of kidney disease and needs further testing. Her slide defines it precisely: 1+ protein on standard dipstick testing, on 2 or more occasions over a 3-month period. Urine can also detect RBCs, WBCs, casts and glucose, and patients with diabetes need to be checked for albuminuria if no protein is seen on routine urinalysis - where she stopped to fix her own slide's missing word: "I think I did a typo there. Patients should have urine checked for albuminuria if routine UA is negative for protein." Renal ultrasound detects obstruction and kidney size, kidney biopsy gives the definitive diagnosis, and GFR is the preferred way to determine kidney function.

The five stages

Slide 44 is a title and a staging table image - it carries no body text, and everything she said on it was off-slide. The criteria below are Lewis's Table 51.7 (p.1239), which is also where the chapter's definition comes from: CKD is either kidney damage or a GFR below 60 mL/min/1.73 m2 for longer than 3 months, and ESRD is a GFR below 15 mL/min, at which point renal replacement therapy is needed to maintain life.

2.15 Conservative Management of CKD

Her four goals: preserve existing kidney function, reduce the risks of cardiovascular disease, prevent complications, and provide comfort. Then referral to a nephrologist and detection and treatment of potentially reversible causes. For stages 1 through 4 the targets are blood pressure control, hyperparathyroidism, CKD-MBD, anemia and dyslipidemia - the list section 2.12 predicts, since the point is to interrupt the cascade before ESRD.

Hyperkalemia

Diet modification comes first on the slide. Lewis's Ch. 17 supplies timing the deck does not: patiromer may take up to 7 hours for initial effect and 2 days for maximal results, which is why it belongs to chronic hyperkalemia rather than to an emergency.

Hypertension, CKD-MBD, hyperparathyroidism and anemia

Lifestyle modification and antihypertensive drugs.ACE inhibitors and ARBs are used in diabetes and in non-diabetic proteinuria - they decrease proteinuria and may delay progression, but are used with caution because they can decrease GFR further and increase hyperkalemia, the same double effect as section 2.8. For bone disease, limit phosphorus to 1 g/day on RRT, give phosphate binders with each meal to bind phosphate in the bowel for excretion in stool (constipation is the side effect), and supplement vitamin D. The caveat that matters: calcium-based binders increase the calcium load and the risk of vascular calcification, so use a non-calcium binder if calcium is high or calcification already exists.

Because the kidneys cannot activate vitamin D, the activated form must be given - calcitriol - and cinacalcet (Sensipar) also helps; if severe, parathyroidectomy may be done to decrease PTH synthesis and secretion. For anemia, exogenous erythropoietin is given IV or subcutaneously 2 to 3 times per week - epoetin alfa (Epogen, Procrit) - and hemoglobin and hematocrit take 2 to 3 weeks to rise. Side effects: increased risk of thromboembolic events and death from serious cardiovascular events, and increased blood pressure.

Transfusion, iron, lipids, drug toxicity and nutrition

The goal is to reduce the need for blood transfusions, avoided unless there is acute blood loss or the patient is symptomatic, because transfusions increase antibody development, making a donor harder to find, and because of iron overload. Iron supplements are IV or oral, with oral limited by GI side effects; they may make stool black and cause constipation, and she gave the teaching behind that - "sometimes black stool can indicate bleeding. So you want to let them know that iron can make this to a black." Statins and fibrates treat dyslipidemia. CKD leads to drug accumulation and potential toxicity, so doses may be adjusted - her drugs of concern are digoxin, metformin and glyburide, vancomycin and opioids.

Protein is restricted, and her slide gives reasoning rather than a number - the body breaks protein into nitrogenous waste the kidneys must filter, and that process is impaired. Refer to a dietician.Fluid is not routinely restricted in CKD stages 1 to 5 in patients not on hemodialysis, though patients on hemodialysis have more fluid restriction than those on peritoneal dialysis, and fluids are spaced through the day so the patient is not thirsty. Restrictions: sodium 2 to 4 g/day, potassium 2000-3000 mg/day, phosphate about 1 g/day at ESRD with meat and dairy the high-phosphate foods. HD patients need potassium restriction; PD patients do not, and salt substitutes must be avoided in a potassium-restricted diet, because they contain potassium chloride.

2.16 Nursing Management of CKD

Assessment: a complete history of kidney disease in the patient or the family, and a medication history - specifically NSAIDs, which can cause AKI and worsen CKD, and magnesium and aluminium from antacids, which the failing kidney cannot excrete. Measure height and weight and evaluate recent weight changes.Assess support systems, an item she stopped to justify because the slide does not: "chronic kidney disease is a difficult disease to deal with. And, um, takes a lot of, a lot of constant care."

Health promotion:identify high-risk persons; check the urine of patients with diabetes for albuminuria if routine urinalysis is negative for protein and teach them to report changes in urine appearance, frequency and volume; monitor kidney function if a nephrotoxic drug is needed; and prevent or delay cardiovascular disease through glycemic control, blood pressure control and lifestyle modification - which she expanded into a list the deck leaves abstract: "diet, exercise, smoking cessation, um, avoid, uh, stopping drug use if that's something they're doing. Um, alcohol use as well. Stress."

Teaching

Teach medications and their side effects, and which OTC drugs to avoid - NSAIDs, and aluminium- and magnesium-based laxatives and antacids. Daily blood pressure readings, and watching for fluid overload, hyperkalemia and other electrolyte imbalances. Evaluation for kidney transplant can be completed ahead of time, which is the stage-4 preparation from section 2.14. And teaching about HD and PD, with education on palliative care.

2.17 Dialysis: What It Is, and How It Works

Dialysis is the movement of fluid and molecules across a semipermeable membrane from one compartment to another - in practice, from the blood into a dialysis solution called the dialysate. The purpose is to correct fluid and electrolyte imbalances and remove waste products, and it can also treat drug overdose. The two types are hemodialysis (HD) and peritoneal dialysis (PD). Dialysis is started when uremia can no longer be managed conservatively, generally at a GFR below 15 mL/min, and certain uremic complications indicate a need for immediate dialysis: encephalopathy, neuropathies, hyperkalemia, pericarditis and accelerated hypertension. She sharpened the slide's "significant mental status change" as she read it - not a change but "a very severe change in mental status."

Most patients with ESRD are treated with dialysis rather than transplant, for three reasons on her slide: lack of donated organs, patients physically or mentally unsuitable for transplant, and patients who do not want one.

2.18 Peritoneal Dialysis, and Its Complications

Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall. It is about 24 inches long with 1 or 2 Dacron cuffs, onto which fibrous tissue grows over a few weeks to hold the catheter in place and prevent bacterial penetration into the peritoneal cavity - she glossed the cuffs as things that "help to anchor the catheter in place so it doesn't move." The perforated tip rests in the peritoneal cavity. It is usually placed surgically so the catheter can be seen directly, and PD can start right after insertion with low-volume exchanges, or be delayed 2 weeks pending healing. Once healed, the patient showers and pats the exit site dry, washes the area with soap and water daily, maintains aseptic technique to avoid peritonitis, and checks the site for infection.

She added that the 2 L is not fixed: it "depends on the patient size um of the peritoneal cavity. They may need less if the peritoneal cavity is smaller; they may need more if it's larger."

The two systems

Automated peritoneal dialysis (APD) uses a machine called a cycler that delivers dialysate and controls fill, dwell and drain. Patients can do it while they sleep - she gave the reason that is safe: "there are machines and alarms and monitors on the machines, so it is safe for patients at night because they'll be awoken by any alarms if, uh, there is an issue." It runs 4 or more exchanges per night at 1 to 2 hours each; the patient disconnects in the morning, fluid stays in the abdomen during the day, and 1 or 2 daytime manual exchanges may be needed. Continuous ambulatory peritoneal dialysis (CAPD) is done every few hours during the day - typically 2 L exchanged 4 times daily with dwells averaging about 4 hours, instilling 2 to 3 L through a disposable administration line that is then disconnected. Her framing is what makes the pair stick: "instead of the cycler machine doing it for the patient, the patient will hook themselves up... They'll do everything pretty much manually."

Complications

Slide 64 was her fifth-longest stop at 460 words, and infection is why. Exit site infection is usually staphylococcus aureus or s. epidermidis from skin flora, presenting as redness, tenderness and drainage; it needs antibiotics, and untreated it progresses to peritonitis. Peritonitis - "an infection in the peritoneal cavity" - results from contact contamination or from an exit site or tunnel infection, and improper technique when connecting tubing during exchanges causes it. Manifestations are abdominal pain, rebound tenderness, cloudy effluent, diarrhea, vomiting, abdominal distention, hyperactive bowel sounds and fever; diagnosis is by culture, gram stain and WBC differential of the effluent; treatment is antibiotics IV, orally or intraperitoneally. Repeated infections cause peritoneal adhesions that interfere with the membrane's ability to act as a dialysing surface, and the catheter may have to be removed.

• Bleeding. It is normal for effluent drained after the first few exchanges to be pink or slightly bloody from insertion trauma, and normal during menstruation. Blood present over several days, or newly appearing, suggests intraperitoneal bleeding and must be evaluated.
• Pulmonary complications.Atelectasis, pneumonia and bronchitis from repeated upward displacement of the diaphragm by the dialysate, which decreases lung expansion. She named the intervention the slide omits: "this is when you can teach the patient about cough and deep breathing."
• Protein loss, because the peritoneal membrane can leak protein from the bloodstream into the dialysate; and hernias and lower back problems from increased intraabdominal pressure from the dialysate volume.

2.19 Hemodialysis: Access, Procedure, Complications, and CRRT

HD requires very rapid blood flow and access to a large blood vessel, and obtaining vascular access is the characteristic problem of hemodialysis. The three types are arteriovenous fistulas (AVFs), arteriovenous grafts (AVGs) and temporary vascular access.

Where her slide stops at "difficult to achieve in some patients," she named who: patients "with histories of peripheral vascular disease, anybody with prolonged IV drug use, or obese patients." She also described what a mature fistula looks like - "it'll be bulging usually like this." A thrill, a buzzing sensation, is felt by palpating the fistula; a bruit, a rushing sound, is heard with a stethoscope.

Temporary catheters go into a vein - her slide says vein, and she says so herself two sentences on, "it's inserted, usually at the bedside, into one of these larger veins." Long-term cuffed catheters can give temporary access while a fistula matures; they tunnel subcutaneously to the internal or external jugular vein with the tip in the right atrium and carry 1 to 2 Dacron cuffs. She named the two device types the deck describes without labelling - a non-tunnelled temporary catheter and a long-term tunnelled catheter - and called the difference "important to know." A hemodialysis reliable outflow (HERO) device is used when other options are exhausted: it bypasses blockages in the central veins with an arterial graft sewn into an artery in the arm and a separate venous outflow component tunnelled under the skin into the right atrium.

The procedure and the dialyzer

Access uses a large-bore 14 to 16 gauge needle: the needle closer to the fistula, red, pulls blood to the machine, and blood is returned through the second needle, blue. When treatment ends, firm pressure is applied to the venipuncture site until bleeding stops - not a formality, since "bleeding can be pretty severe because of that high level of flow through that vein." Before treatment, assess fluid status (weight, BP, peripheral edema, lung and heart sounds), the vascular access and the temperature. The difference between the last post-dialysis weight and the present pre-dialysis weight determines the ultrafiltration - how much fluid to remove. Check vital signs every 30 to 60 minutes, because rapid blood pressure changes can occur. Schedules are 3 to 4 hours about 3 days a week in a centre, nocturnal HD of 6 to 8 hours up to 6 times a week, short daily treatments of 2.5 to 3 hours 5 to 6 times a week, and home HD, which she said "is not very commonly seen."

The dialyzer is a plastic cartridge of thousands of parallel hollow semipermeable fibres. Blood is pumped into the top and dispersed into the fibres; dialysate is pumped into the bottom and bathes the outside of them.Ultrafiltration, diffusion and osmosis occur across the pores, and the dialysed blood converges into a single lumen tube that returns it to the patient. Because blood clots on contact with the foreign material of the dialyzer, heparin is added - one of only three things she called important to know.

Complications, effectiveness, and CRRT

Hypotension is the first complication on her slide: it occurs from rapid removal of volume, producing hypovolemia, decreased cardiac output and decreased systemic vascular resistance, with lightheadedness, nausea and vomiting, seizures, vision changes or chest pain, and is treated by infusing 0.9% saline. The rest are muscle cramps, loss of blood, and hepatitis from exposure to possibly infected equipment. On effectiveness her slide is blunt: HD cannot fully replace the normal biologic functions of the kidneys; it eases symptoms and prevents complications of CKD if started early but does not alter the accelerated rate of cardiovascular disease. Patients may become nonadherent, depressed, or show suicidal tendencies, and the key nursing goals are a healthy self-image and the highest possible level of function. She gave the concrete reason adherence fails - a Monday-Wednesday-Friday or Tuesday-Thursday-Saturday schedule "makes it difficult for them to really go anywhere."

CRRT is a method for treating AKI - note that this slide closes the dialysis block but the therapy belongs to the acute patient. It dialyses in a more physiological way, over 24 hours, similar to the kidneys, and is contraindicated when the patient has life-threatening manifestations of uremia such as hyperkalemia or pericarditis that need rapid treatment, because slow is exactly what those patients cannot afford. It can be used together with HD, and access is a double-lumen catheter in the jugular or femoral vein.

2.20 Kidney Transplant

She gave transplant about nine minutes across nine slides, her lightest treatment of any block, and read it closely. Transplant is the best treatment option for ESRD, but fewer than 4% of patients have one - and she gave the reason, not on the slide: "this is due to the high number of people on the transplant list." About 24,000 transplants take place each year.One-year survival is over 90% for deceased donor and 95% for live donor transplants. Transplant reverses many of the pathophysiologic changes of renal disease and eliminates dependence on dialysis. Her slide dates the first live donor transplant to 1954; she did not mention it.

Donors may be compatible-blood-type deceased donors, blood relatives, emotionally related living donors, or altruistic living donors. Live donors account for 27% of US kidney transplants, undergo extensive evaluation - she added psychological evaluation, which the slide does not - and have crossmatches at evaluation and again the week before transplant. A live donor gives better patient and graft survival, immediate organ availability, immediate function from minimal cold time, and the chance to have the recipient in the best possible health. Deceased donors are fairly healthy people with irreversible brain injury declared brain dead, and even with a signed donor card, permission from the next of kin is still requested. Kidneys are preserved for up to 72 hours, though some surgeons prefer to transplant before cold time reaches 24 hours, and prolonged cold time increases the chance the kidney will not function immediately.

• Preoperatively: emotional and physical preparation, with teaching that stresses the kidney may not function at once and dialysis may be needed for days to weeks. ECG, chest x-ray and labs; dialysis may be needed before surgery to remove fluid or potassium. Maintain the vascular access and label the extremity "dialysis access, no procedures" - the same limb rule as section 2.19.
• Live donor postoperatively: monitor renal function and hematocrit. Donors usually have more pain than recipients.Open approach - 4 to 5 days in hospital, back to work in 6 to 8 weeks; laparoscopic - 2 to 4 days, back to work in 4 to 6 weeks, and she noted "most of the time nowadays laparoscopic is more common." Acknowledge the gift this person has given.
• Recipient postoperatively:maintain fluid and electrolyte balance, 12 to 24 hours in ICU, expect large volumes of urine, monitor central venous pressure, avoid dehydration to prevent renal hypoperfusion and tubular damage. ATN can occur in the transplanted kidney from prolonged cold time, and dialysis is needed while it persists - she added that it "will usually improve, but it can last for days to weeks." Dialysis stops when urine output increases and creatinine and BUN begin to normalise.
• A sudden decrease in urine output in the early postoperative period is concerning - from dehydration, rejection, urine leak or obstruction. A blood clot in the urinary catheter can be the obstruction, so

maintain catheter patency; she added that the physician "may order some irrigation of the catheter and bladder if these clots continue to form." Immunosuppressive therapy prevents rejection.

Her closing list of complications is six items: rejection, infection, cardiovascular disease, cancers, recurrence of the original kidney disease, and corticosteroid-related complications. She supplied the causal link the list omits for two - infection "because also they're on immunosuppressive agents," and corticosteroid complications because "most kidney transplant patients are placed on steroids." Both follow from the regimen that keeps the graft alive, which is the tension the whole postoperative course manages.

Her final slide is "Questions?" She never read it. What she said instead was the disposition for the entire deck, and for the two application slides in section 2.9: "All right, that's it. So I'll go ahead and upload this and then we'll go over it in class."

3.1 Background: Type 1, Type 2, and the Diagnostic Numbers

Type 1 diabetes is caused by insulin deficiency following destruction of the insulin-producing pancreatic beta cells. It most commonly appears in children, but a quarter of cases are diagnosed in adults. She added the word her slide leaves out: the beta cells "are being destroyed by some type of autoimmune process."

Type 1 presents in one of three ways: the classic new onset of polydipsia, polyuria and weight loss with hyperglycemia and ketonemia; as DKA; or silently, as an incidental discovery. Treatment is insulin injections plus lifestyle modification.

Type 2 diabetes is characterized by hyperglycemia, insulin resistance, and a relative impairment in insulin secretion - as opposed to type 1, which is little to no production at all. Risk factors are obesity and family history on her slide; she added smoking. Symptoms are polydipsia, polyphagia, polyuria, unexplained weight loss, slow-healing sores, yeast infections and fatigue. Treatment moves through lifestyle modification, oral medications, and insulin.

Diagnostic criteria - the same for type 1 and type 2

3.2 Hyperglycemia and Hypoglycemia: The Acute Complications

Her framing for the whole slide: complications arise from events associated with hyperglycemia and hypoglycemia. Hyperglycemia is not enough insulin working. Hypoglycemia is too much insulin working. That sentence pair is the reason the two lists of causes look the way they do.

3.3 DKA: Who Gets It and Why

Diabetic ketoacidosis is caused by a profound deficiency in insulin. It is characterized by four things - hyperglycemia, ketosis, acidosis and dehydration - and every one of the four is a separate treatment target later.

DKA is more likely to occur in people with type 1 diabetes, but it can still occur in type 2 in conditions of severe illness or stress in which the pancreas cannot meet the insulin demand. She said only that it "can occur in patients with type two diabetes as well, but it's more common in type one" - the why is on the slide.

Precipitating factors

• Illness
• Infection
• Inadequate insulin dosage
• Undiagnosed type 1 diabetes - the first presentation is the DKA
• Lack of education or understanding
• Lack of resources, or neglect

3.4 DKA Pathophysiology: Why Ketones Form

This is the chain her slide prints and she walked. Learn it as a chain, because the treatment order in 3.6 and 3.7 follows it.

• The circulating supply of insulin is insufficient, so glucose cannot be used for energy.
• The body breaks down fat stores for fuel.
• Ketones are produced as by-products of fat metabolism.
• Ketosis alters the pH balance and metabolic acidosis develops.
• Meanwhile, insulin deficiency stimulates glucose production in the liver, worsening the hyperglycemia.
• And the insulin deficiency means the body still cannot use that new glucose, worsening the hyperglycemia again.
• The rising glucose adds to the osmotic diuresis.
• Ketones are excreted in the urine - ketonuria.

3.5 DKA: Clinical Manifestations and the Lab Numbers

The DKA lab values

3.6 DKA Treatment, Part 1: Fluids

Whether the patient is hospitalized depends on presentation. She was specific about the real-world split: "they can possibly be monitored as an outpatient if they are stable enough to be. But if they're coming to the emergency room, they're usually not stable enough to be treated at home." The chapter agrees and adds the deciding factors: fever, nausea, vomiting and diarrhea; altered mental status; the cause of the DKA; and whether the patient can reach the provider every few hours. A patient with DKA plus pneumonia or a UTI is usually admitted.

Assess mental status first, then begin fluids. IV fluid management uses 0.45% or 0.9% normal saline - she called 0.45% by its spoken name, half normal saline. The chapter adds the endpoint that tells you the fluids are working: infuse at a rate that raises the blood pressure and restores urine output to 30-60 mL/hr.

Dextrose at 250 - and the cerebral edema risk

When glucose levels approach 250 mg/dL, 5% to 10% dextrose is added to the IV fluids to prevent hypoglycemia. The reason is that the insulin drip is still running - the acidosis, not the glucose, is what determines when insulin stops, so the dextrose is what keeps the patient safe while the insulin finishes its real job.

Electrolytes, monitoring and the ECG

• Electrolyte therapy corrects deficits in sodium, chloride, bicarbonate, potassium, phosphate and magnesium. She named sodium chloride, bicarbonate, potassium "or any other electrolytes" - phosphate and magnesium are on the slide only.
• Record intake and output.
• Monitor blood glucose levels.
• ECG monitoring. Her slide gives the words with no reason; she gave it: "if they have electrolyte imbalances, that can cause arrhythmias, such as with hypo- or hyperkalemia." Potassium is a cardiac drug as much as an electrolyte, which is the whole justification for section 3.7.

3.7 DKA Treatment, Part 2: The Potassium Rule and Insulin

Obtain a serum potassium before starting insulin. If the patient is hypokalemic, insulin will further the problem by dropping the potassium even lower, so potassium replacement is essential.

• Sequence she stated: "usually if the potassium is low, the provider will replace that potassium before the insulin drip is started." Potassium first, then insulin.
• The nurse's task, in her words: check the level and make sure the provider knows it. The communication step is part of the intervention.
• IV insulin is given to correct the hyperglycemia and hyperketonemia - both, which is why it does not stop when the glucose normalises.
• Rapid drops in glucose can cause cerebral edema.
• A glucose reduction of 36-54 mg/dL/hr will avoid complications. That is the target rate, and it is the number behind the titration.
• Monitor fluid balance and potassium levels.
• She described the drip as continuous and around the clock: "this is a continuous insulin drip through the IV."

What happens if DKA is not treated

Her slide gives the cascade and she walked it: severe depletions in electrolytes →hypovolemia→shock→ renal failure from shock→ retention of glucose and ketones →increased acidosis→ the patient becomes comatose from dehydration, electrolyte imbalance and acidosis. Death is inevitable if it is not treated. She supplied the missing link in the middle: "shock can prevent blood flow to the kidneys, which could cause renal failure."

3.8 HHS: Pathophysiology and Why There Are No Ketones

Hyperosmolar hyperglycemia syndrome is a life-threatening syndrome occurring in patients with diabetes who are able to make enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion. It is less common than DKA, and it often occurs in patients over 60 with type 2 diabetes. Common causes: UTI, pneumonia, sepsis, acute illness, and newly diagnosed type 2 diabetes.

The osmotic mechanism, step by step

• Glucose is an osmotically active solute - meaning water follows glucose.
• Glucose levels rise in the blood, so water is pulled out of the cells into the blood.
• Normally the kidneys hold on to the body's glucose. In this state of hyperglycemia they cannot hold any more, and glucose spills into the urine - glucosuria.
• Water follows the glucose into the urine, and the body loses fluid.
• With the water gone, the concentrations of sodium, potassium and glucose all rise, because there is less water left to dilute them. This is hyperosmolality.
• It is usually compounded by an impaired thirst sensation, so the patient does not drink to replace the loss - and the dehydration becomes profound.

3.9 HHS: Manifestations, Labs, and the Stroke Mimic

HHS has fewer symptoms in the earlier stages and can reach very high glucose levels before it is identified. The higher glucose raises serum osmolality, and the higher the osmolality, the more severe the neurologic manifestations: coma, somnolence, seizures, hemiparesis, aphasia. Those symptoms resemble a stroke.

She also added an attribution the slide does not make: the neurologic changes track sodium specifically - "some of these elevations in some of these electrolytes can cause neurological symptoms, usually related to sodium levels." And she noted, where the slide marks the osmolality rise as an HHS finding, that "you want to monitor the serum osmolality, because as we know, that increases in DKA and HHS."

3.10 HHS: Management

HHS is a medical emergency with a high mortality rate, and management is similar to DKA - IV fluids, IV insulin, and electrolyte correction. Two things change, and both changes come from the population: these patients are older and sicker.

• Fluid overload is the specific danger. Patients with HHS are usually older and may have comorbidities like heart or kidney problems, so fluid replacement requires monitoring to avoid overload. She named the exemplar comorbidity where the slide says only "heart or kidney problems": heart failure.
• Hypokalemia is not as significant in HHS as it is in DKA. The chapter explains why in a way her slide does not: without the acidosis and the profound insulin deficiency, the potassium shifts are smaller - though fluid losses still produce milder potassium deficits that require replacement.
• Once the patient is stable, detect and correct the underlying cause. Her examples, where the slide gives only the instruction: "whether it be infection, whether it be illness, noncompliance to medications, things of that sort."
• The chapter adds the volume detail: HHS usually requires large volumes of fluid replacement, given slowly and carefully, and dextrose is added when the glucose falls to about 250 mg/dL - the same threshold as DKA.

3.11 DKA versus HHS, Side by Side

This is the single most useful table in the unit, because almost every distinguishing feature can be derived from one root fact: DKA has essentially no insulin, HHS has a little.

3.12 Complications of Treatment

Everything in this section is iatrogenic - these are the harms produced by treating the syndrome, which is why they are nursing responsibilities rather than medical ones. Each has a specific monitoring parameter attached.

3.13 Nursing Management and Patient Education

Her final slide covers both syndromes together. The nursing role here is almost entirely monitoring, and each parameter exists to catch one of the complications in 3.12.

Her single line about potassium on this slide is the restatement of the 3.7 rule: when insulin treatment is started, potassium levels may decrease rapidly. That sentence is the reason every other monitoring parameter on the slide exists in the order it does.

Glossary

Definitions here follow her slides and her spoken definitions wherever she gave one. Where a term appears only in Lewis, the entry says so.

Part 1 - Abbreviations

Part 2 - Key Terms

1.1 The Three Intracranial Volume Components

The cranial vault holds three things, and only three. Their proportions are worth memorizing because the compensation story depends on which one has room to give.

1.2 Normal Intracranial Pressure

Intracranial pressure (ICP) is the hydrostatic force measured in the brain's CSF compartment. Under normal conditions the total intracranial volume stays relatively constant and the balance among the three components holds pressure steady.

• Normal ICP = 5 to 15 mm Hg.
• A sustained pressure above 20 mm Hg is abnormal and is the threshold most treatment protocols are written around.
• ICP can be measured in the ventricles, subarachnoid space, subdural space, epidural space, or brain tissue using a pressure transducer.

Six factors influence ICP even in a healthy person. How much each one actually moves the pressure depends on how much adaptive capacity the brain has left.

1.3 The Monro-Kellie Doctrine

The Monro-Kellie doctrine states that the three components must stay at a relatively constant total volume within the closed skull. If the volume of one component increases and volume from another component is displaced, total intracranial volume does not change - and pressure does not rise.

1.4 Compensation - and Decompensation

The body adapts to a rising volume in three ways, in roughly this order of speed and availability:

• Changes in CSF volume - altering CSF absorption or production, and displacing CSF out of the cranium into the spinal subarachnoid space.
• Changes in intracranial blood volume - collapse of cerebral veins and dural sinuses, regional cerebral vasoconstriction or dilation, and changes in venous outflow.
• Changes in brain tissue volume - distention of the dura, or compression of brain tissue itself.

Initially, an increase in volume does not raise ICP, because these mechanisms absorb it. But compensation is limited. As volume keeps increasing, the reserve runs out, ICP begins to climb, and the patient decompensates - leading to compression and ischemia. The clinical shape of this is a flat curve followed by a steep one: small further increases in volume now produce large increases in pressure.

1.5 Primary Versus Secondary Brain Injury

This distinction organizes the entire management chapter, because only one of the two is something nursing care can change.

1.6 Cerebral Blood Flow and What Controls It

Cerebral blood flow (CBF) is the amount of blood in milliliters passing through 100 g of brain tissue in one minute. Global CBF is about 50 mL/min/100 g.

The brain has almost no metabolic reserve. It requires a constant supply of oxygen and glucose, and it consumes 20% of the body's oxygen and 25% of its glucose - a disproportionate share for an organ that is about 2% of body weight. That is why even brief interruptions in flow produce injury.

Carbon dioxide, oxygen, and the acid loop

Severely low PaO2 and an increased hydrogen ion concentration are both potent cerebral vasodilators. Together they can produce a state in which autoregulation is lost and compensatory mechanisms can no longer meet the tissue's metabolic demand. Once autoregulation is gone, CBF is directly at the mercy of systemic BP, hypoxia, and catecholamines.

• Global CBF is affected by cardiac or respiratory arrest, systemic bleeding, and other whole-body states - diabetic coma, infections, toxicities.
• Regional CBF is affected by trauma, tumors, cerebral bleeding, and stroke.

1.7 Autoregulation

Cerebral autoregulation is the automatic adjustment in the diameter of cerebral blood vessels that maintains a constant blood flow despite changes in arterial blood pressure. Its purpose is to guarantee consistent CBF for metabolic needs and to keep cerebral perfusion pressure within normal limits.

• Lower limit of effective autoregulation = MAP of 70 mm Hg. Below this the vessels are already maximally dilated, CBF falls, and cerebral ischemia produces syncope and blurred vision.
• Upper limit = MAP of 150 mm Hg. Above this the vessels are maximally constricted and the vasoconstrictor response is lost - further rises in pressure are transmitted straight into the brain.

1.8 Cerebral Perfusion Pressure - the Number That Decides

Cerebral perfusion pressure (CPP) is the pressure needed to ensure blood flow to the brain. It is the difference between the pressure pushing blood in and the pressure inside the skull resisting it.

• Normal CPP = 60 to 100 mm Hg. Treatment goal in increased ICP is to maintain CPP greater than 60 mm Hg.
• CPP <50 mm Hg - associated with ischemia and neuron death.
• CPP <30 mm Hg - ischemia incompatible with life.

Two refinements the chapter adds. First, cerebrovascular resistance - generated by arterioles inside the cranium - links pressure and flow: CPP = Flow x Resistance. When cerebrovascular resistance is high, blood flow to brain tissue is impaired even at an apparently adequate CPP. Second, CPP is a global number and may not reflect perfusion in every part of the brain; local swelling and compression limit regional perfusion. Such patients may need a higher CPP than normal to prevent localized tissue damage - a patient with acute stroke, for instance, may need a higher BP to raise MAP and CPP and so increase perfusion to threatened tissue.

2.1 What Increased ICP Is and Why It Is Lethal

Increased ICP is potentially life threatening and results from an increase in any or all of the three components inside the skull. It is clinically significant for one reason: it decreases cerebral perfusion pressure and therefore increases the risk for brain ischemia and infarction. Prognosis is poor once it is established.

The two common causes are a mass - hematoma, contusion, abscess, tumor - and cerebral edema, which arises from brain tumors, hydrocephalus, head injury, and brain inflammation.

2.2 The Cascade - Learn It as a Loop

The reason increased ICP is so dangerous is that it feeds itself. The chapter lays the progression out as a closed circuit; this is the single most useful mechanism in the whole neuro unit because almost every manifestation and almost every intervention attaches to a step in it.

2.3 Cerebral Edema

Cerebral edema is an increased accumulation of fluid in the extravascular spaces of brain tissue, which increases tissue volume and therefore ICP. The extent and severity of the original insult determine the degree of edema, and a single patient may have more than one type at once.

Cerebral insults increase both the formation and the spread of edema, and may produce hypercapnia, cerebral acidosis, impaired autoregulation, and systemic hypertension. The edema distorts brain tissue, which raises ICP further, which worsens tissue hypoxia and acidosis - the loop again.

2.4 The Three Types of Cerebral Edema

2.5 Causes of Cerebral Edema

2.6 Herniation - the Endpoint

Sustained increases in ICP lead to brainstem compression and brain herniation. Herniation is brain tissue forcibly shifted from a compartment of greater pressure into a compartment of less pressure. It turns a potentially reversible process into an irreversible one, because ischemia and edema increase in the herniated tissue, compounding the original problem.

Herniation forces the cerebellum and brainstem downward through the foramen magnum. If brainstem compression is not relieved, the patient arrests - respiratory arrest from compression of the respiratory control center in the medulla. Continued herniation means brainstem death is imminent.

The anatomy you need

• Falx cerebri - a thin wall of dura folding down between the cortex, separating the two cerebral hemispheres.
• Tentorium cerebelli - a rigid fold of dura separating the cerebral hemispheres from the cerebellum. Named for a tent, because it forms a tent-like cover over the cerebellum.

3.1 Change in Level of Consciousness - the Earliest Sign

Level of consciousness is the most sensitive and reliable indicator of neurologic status. It changes before the vital signs change, before the pupils change, and before the motor exam changes. If you learn one priority from this chapter, learn this one.

The mechanism - why LOC is the first thing to go

Changes in LOC result from impaired cerebral blood flow, which deprives the cells of the cerebral cortex and of the reticular activating system (RAS) of oxygen. The RAS lies in the brainstem with connections throughout the nervous system; an intact RAS can maintain wakefulness even without a functioning cerebral cortex. Interruption of RAS impulses, or a change in cerebral hemisphere function, produces unconsciousness - an abnormal state of complete or partial unawareness of self or environment.

• The change may be dramatic - coma - or subtle: flattening of affect, a change in orientation, a decreased level of attention. The subtle version is the one that gets missed.
• State of consciousness is defined both by clinical responses and by the pattern of brain activity on EEG.
• In the deepest state (coma): no response to painful stimuli; corneal and pupillary reflexes absent; cannot swallow or cough; incontinent of urine and feces; EEG shows suppressed or absent neuronal activity.

3.2 Changes in Vital Signs - Cushing's Triad (a Late Sign)

Vital sign changes are caused by increasing pressure on the thalamus, hypothalamus, pons, and medulla. They are late. They often do not appear until ICP has been elevated for some time, or until it rises suddenly and markedly, as in head trauma.

Worked example - reading a set of vital signs

An 82-year-old woman fell and struck her head on a fire hydrant. On admission she was confused, with BP 150/86, pulse 84, respirations 14/min. Two hours later: BP 166/74, pulse 54, respirations 10-16/min.

• Pulse pressure went from 64 to 92 - widening, and the systolic rose while the diastolic fell.
• Pulse fell from 84 to 54 - bradycardia.
• Respirations became slow and irregular, ranging 10-16.
• All three legs of the triad are present. Interpretation: increasing ICP with brainstem compression. This is a medical emergency; notify the health care provider immediately.

3.3 Ocular Signs

The pupil findings in increased ICP come from one nerve being squeezed. As the brain shifts from the midline it compresses the trunk of cranial nerve III (oculomotor), paralyzing the muscles that control pupillary size and shape.

3.4 Decrease in Motor Function and Posturing

Contralateral hemiparesis or hemiplegia - weakness on the side opposite the mass lesion - may develop, depending on location. With painful stimuli, a patient may localize to the stimulus or withdraw from it; those are better responses than posturing.

A patient may show decorticate posturing on one side and decerebrate on the other, or opisthotonic posturing - the whole body arched. A change from decorticate to decerebrate is deterioration: the injury has moved deeper, from cortex to brainstem.

3.5 Headache and Vomiting

• Headache. The brain itself is insensitive to pain; the headache comes from compression of other intracranial structures - arteries, veins, and cranial nerves. A nocturnal headache and/or a morning headache is cause for concern and may indicate a tumor or other space-occupying lesion. Straining, agitation, or movement worsens the pain - because all of them raise ICP further.
• Vomiting. Unexpected vomiting - vomiting not preceded by nausea - is a nonspecific sign of increased ICP related to pressure changes in the cranium. Projectile vomiting may occur and is likewise related to increased ICP.

3.6 Abnormal Respiratory Patterns in Coma

The breathing pattern localizes the lesion, because different levels of the brainstem drive respiration differently. Charting "irregular" loses that information - name the pattern.

4.1 Diagnostic Studies

• CT and MRI - the workhorses. They identify most conditions causing increased ICP and assess the effect of treatment.
• Also used: EEG, cerebral angiography, ICP measurement, brain tissue oxygenation via a LICOX catheter, PET, transcranial Doppler, and evoked potential studies.
• Transcranial Doppler monitors changes in cerebrovascular resistance.
• Infrascanner - a hand-held near-infrared scanner used in some agencies to detect life-threatening intracranial bleeding. It directs a wavelength of light that penetrates tissue and bone; blood from an intracranial hematoma absorbs light differently from other brain areas.
• Labs: CBC, coagulation profile, electrolytes, serum creatinine, ABGs, ammonia level, drug and toxicology screen; CSF analysis for protein, WBC, and glucose.

4.2 Management Targets

These are the numbers the interprofessional plan is written around. Memorize them as a set; a question that hands you a value is usually asking whether you recognize it as inside or outside the target.

Beyond the numbers: mechanical ventilation as needed, ICP monitoring, cerebral oxygenation monitoring (PbtO2, SjvO2), maintenance of fluid balance with assessment of osmolality, and reduction of cerebral metabolism, for example with high-dose barbiturates. If increased ICP is caused by a mass - a tumor or hematoma - surgical removal is the best treatment; in aggressive situations a craniectomy may be done to reduce ICP and prevent herniation.

4.3 Indications for ICP Monitoring

• Used to guide care when a patient is at risk for or has increased ICP - stroke, hemorrhage, tumor, infection, traumatic brain injury.
• ICP should be monitored in patients admitted with a GCS score of 8 or less AND an abnormal CT scan or MRI indicating possible bleeding, contusion, edema, or other problems.
• Performed in the ICU, except in patients with irreversible problems or advanced neurologic disease.

4.4 Methods of Measuring ICP

Reading the number

• ICP is displayed as a mean pressure in mm Hg.
• If a CSF drainage device is in place, the drain must be CLOSED for at least 6 minutes to ensure an accurate reading.
• Record the waveform strip along with other pressure waveforms; monitor both the ICP waveform and the mean CPP.
• Neurologic deterioration may not occur until the ICP increase is pronounced and sustained. Consider the rate at which changes occur, not just the value.
• Report to the health care provider immediately any increase in ICP - either a rise in mean pressure or an abnormal waveform configuration.

4.5 ICP Waveforms

When ICP is normal, P1, P2, and P3 descend like a staircase. As ICP rises, P2 climbs above P1 - the signature of poor ventricular compliance, and often the earliest monitored warning that the brain has run out of reserve. At very high ICP the peaks lose definition and the waveform plateaus.

Causes of an inaccurate reading

• CSF leaks around the monitoring device
• Obstruction of the intraventricular catheter by tissue or blood clot
• A difference between the height of the catheter and the transducer
• Kinks in the tubing
• Incorrect height of the drainage system relative to the patient's reference point
• Bubbles or air in the tubing, which dampen the waveform

Infection - the serious complication of monitoring

• Contributing factors: ICP monitoring for more than 5 days, use of a ventriculostomy, a CSF leak, and a concurrent systemic infection.
• Nursing prevention: routinely assess the insertion site, use aseptic technique, and monitor CSF for a change in drainage color or clarity.

4.6 Cerebrospinal Fluid Drainage

With a ventricular catheter in place, ICP can be controlled by removing CSF. The provider orders a specific level at which to start drainage - commonly ICP >20 mm Hg - and the frequency, intermittent or continuous. There are no universal guidelines for CSF removal; practice follows agency or provider preference.

• Intermittent drainage: open the system at the indicated ICP, allow CSF to drain for 2 to 3 minutes - brief periods of 30 to 120 seconds - until pressure falls below the upper parameter, then close the stopcock to return the ventriculostomy to a closed system.
• Continuous drainage: carefully monitor the volume of CSF drained.
• Reference values: normal CSF production ~ 20 to 30 mL/hr; total CSF volume ~ 150 mL in the ventricles and subarachnoid space. Against a 150 mL total, over-drainage happens fast.
• Post a sign above the patient's bed to notify anyone before turning, moving, or suctioning the patient - to prevent removal of too much CSF, which causes serious complications.
• Complications of CSF drainage: ventricular collapse, infection, and herniation or subdural hematoma formation from rapid decompression.
• Use strict aseptic technique during dressing changes and CSF sampling, and keep the system intact so readings stay accurate - treatment is based on those pressures.

4.7 Cerebral Oxygenation Monitoring

ICP tells you the pressure. It does not tell you whether the tissue is actually getting oxygen. Three ICU devices answer that second question.

4.8 Drug Therapy for Increased ICP

4.9 Metabolic Demands and Nutrition

Anything that raises the brain's metabolic rate raises its oxygen demand, its blood flow, and therefore its pressure. The chapter names five: fever (>100.4°F [38°C]), agitation, shivering, pain, and seizures.

• Maintain temperature at 96.8°F to 98.6°F (36°C to 37°C).
• Do not let the patient shiver. Shivering increases the metabolic workload on the brain - it defeats the cooling that provoked it. If it occurs, the patient may need sedatives or a different cooling method.

Nutrition

• Malnutrition promotes continued cerebral edema, so optimal nutrition is not optional.
• The patient with increased ICP is in a hypermetabolic and hypercatabolic state that increases the need for glucose as fuel for the injured brain.
• If oral intake is inadequate, use enteral feedings or parenteral nutrition.
• Early feeding after brain injury may improve outcome. Nutrition replacement should meet caloric needs by at least day 5 after injury.
• Keep the patient in a EUVOLEMIC fluid state. Continuously evaluate urine output, insensible fluid loss, serum and urine osmolality, and serum electrolytes.

5.1 The Glasgow Coma Scale

The GCS is a quick, practical, standard system for assessing level of consciousness. It scores three abilities: the patient's ability to open the eyes to a verbal or painful stimulus, to speak, and to obey commands - recorded as eye opening, best verbal response, and best motor response.

• Your responsibility is to elicit the BEST response on each scale. Not the first response, not the average - the best.
• Subscale scores matter especially when a patient is untestable in one area - severe periorbital edema, for instance, makes eye opening impossible to score.
• Total = sum of the three areas. Highest = 15 (fully alert). Lowest = 3. A GCS of 8 or less generally indicates COMA.
• Higher scores mean a higher level of brain functioning. Plot GCS scores on a graph to see whether the patient is stable, improving, or deteriorating - the trend carries more information than any single score.
• Advantage: different clinicians reach the same conclusion about status, and the scale distinguishes between different or changing states.

* "Untestable" was added to the original scale by some centers.

Other scales the chapter names: the FOUR (Full Outline of UnResponsiveness) scale, and, for stroke or hemorrhage with increased ICP, the NIH Stroke Scale. Cranial nerve assessment and motor and sensory testing accompany any of them.

5.2 Neurologic Assessment at the Bedside

Eye movements and brainstem reflexes

• Assess movements controlled by CN III, IV, and VI in the awake patient who can follow commands - this is a test of brainstem function.
• Corneal reflex tests CN V and CN VII. If it is absent, start routine eye care to prevent corneal abrasion.
• Oculocephalic reflex (doll's eye) - turn the head briskly left or right while holding the eyelids open. Normal: the eyes move across the midline in the direction OPPOSITE the turn. Then flex and extend the neck: the eyes move opposite to the head - up when the neck is flexed, down when it is extended. Abnormal responses help localize a lesion. Usually done only as part of the evaluation of brain death.
• Oculovestibular reflex (cold caloric) - with the head of the bed elevated, instill a syringe of ice-cold water into the external auditory canal and assess the eyes for a total of 1 minute. Absence of eye movement or response indicates severe neurologic demise. Requires patent external auditory canals and intact tympanic membranes.

Motor assessment

• Test all four extremities for strength and note asymmetry in strength or movement.
• In the unconscious or uncooperative patient, observe spontaneous movement; if there is none, apply a pain stimulus and note the response. Resistance to movement during passive range of motion is another measure of strength.

5.3 Respiratory Function - the First Priority

Maintaining a patent airway is critical and a major nursing responsibility. As LOC decreases, the risk of airway obstruction rises - from the tongue dropping back and occluding the airway and from the accumulation of secretions.

• Suction as needed. An oral airway facilitates breathing and provides an easier suctioning route in the comatose patient.
• Frequently monitor and evaluate ABG values; ventilatory support is ordered based on PaO2 and PaCO2.
• Prevent hypoxia and hypercapnia to minimize secondary injury - both are steps in the ICP loop.

Suctioning rules

The mechanism behind every rule below is the same: suctioning and coughing cause transient decreases in PaO2 and increase ICP, and patients with raised ICP are at risk for a lower CPP during suctioning.

• Prevent abdominal distention, which interferes with respiratory function. An NG tube to aspirate stomach contents prevents distention, vomiting, and aspiration.
• Contraindication: in patients with facial and skull fractures, an NG tube is contraindicated because of the risk for inadvertent INTRACRANIAL placement. Oral insertion of a gastric tube is preferred.

5.4 Sedation and Analgesia

Pain, anxiety, and fear - from the primary injury, from therapeutic procedures, or from noxious stimuli - increase ICP and BP. Treating them is treatment for the pressure, not a comfort measure bolted on afterward.

But sedatives, paralytics, and analgesics may alter the neurologic state and mask true neurologic changes. It may be necessary to temporarily stop drug therapy in order to assess neurologic status appropriately. Choice, dose, and combination vary with history, neurologic state, and clinical presentation.

Environment matters as much as pharmacology: keep it quiet and calm with minimal noise and interruptions. Observe for signs of agitation, irritation, and frustration. Teach the caregiver and family about decreasing stimulation, and coordinate with team members to minimize procedures that may cause agitation - clustering care is a pressure intervention.

5.5 Fluid and Electrolyte Balance

• Closely monitor IV fluids with an accurate infusion control device or pump.
• Intake and output, accounting for insensible losses, and daily weights assess fluid balance.
• Monitor serum electrolytes - especially glucose, sodium, potassium, and magnesium - and osmolality. Discuss abnormal values with the provider.

Urine output is the early clue to two opposite complications of intracranial injury, both driven by antidiuretic hormone. Watch the volume, then confirm with the sodium.

5.6 Body Position

Positioning is the cheapest ICP intervention there is, and the chapter states it as a set of rules with a built-in tension between ICP and CPP.

• Maintain the patient in the HEAD-UP position. Elevating the head of the bed promotes drainage from the head and decreases the vascular congestion that produces cerebral edema.
• Keep the head in a MIDLINE (neutral) position and avoid extreme neck flexion - flexion causes venous obstruction and contributes to increased ICP.
• However: raising the head of the bed MORE THAN 30 DEGREES can DECREASE CPP by lowering systemic BP. Carefully evaluate the effect of head elevation on both ICP and CPP, and position the bed so it lowers ICP while optimizing CPP and other indices of cerebral oxygenation.
• Turn the patient with slow, gentle movements - rapid position changes may increase ICP.
• Prevent discomfort when turning or positioning - pain or agitation increases pressure.
• Avoid extreme hip flexion, which raises intraabdominal pressure and therefore ICP.
• Turn the patient at least every 2 hours to minimize the complications of immobility - atelectasis and contractures.
• Decorticate or decerebrate posturing is a reflex response in some patients: turning, skin care, and even passive range of motion can elicit it.

Two related rules follow from the same physiology. Increased intrathoracic pressure increases ICP by impeding venous return, so the patient should avoid coughing, straining, sneezing, and the Valsalva maneuver. And be alert to the other factors that raise ICP so you can minimize them: suctioning, hypoxemia, and arousal from sleep.

5.7 Protection From Injury

Patients with increased ICP and decreased LOC need protection from self-injury, because confusion, agitation, and the possibility of seizures all increase risk.

• Use restraints carefully. If restraints are needed to keep the patient from removing tubes or falling out of bed, they must be secure enough to be effective, and you must observe the skin under them regularly for irritation.
• Agitation may INCREASE with restraints - that is a signal that other measures are needed. Light sedation may help; having a family member stay may have a calming effect.
• Seizure precautions: padded side rails, an Ambu bag at the bedside, readily available suction, accurate and timely administration of antiseizure drugs, and close observation.
• Antiseizure prophylaxis against EARLY seizures - within the first 7 to 10 days - is recommended in SEVERE brain injury. It is controversial for mild to moderate brain injury.
• Provide a quiet, nonstimulating environment and a calm, reassuring approach. Touch and talk to the patient, even one who is in a coma.

5.8 Psychologic Care and Evaluation

• Provide support, information, and teaching to both patients and families. Anxiety about diagnosis and prognosis is distressing to patient, caregiver, family, and staff alike.
• A competent and assured manner is reassuring. Give short, simple explanations, and allow the patient and caregiver to acquire the amount of information they desire.
• Assess family members' desire to help provide care and allow their participation as appropriate. Involve social work and chaplaincy, and include patient and family in decision making as much as possible.

Expected outcomes. The patient will maintain ICP and cerebral perfusion within normal parameters, have no serious increases in ICP during or after care activities, and have no complications of immobility.

6.1 Definitions and Scale of the Problem

Head injury is any injury or trauma to the scalp, skull, or brain. Its serious form is traumatic brain injury (TBI).

• About 2.8 million people are treated each year in US emergency departments for TBI. Of those, 57,000 die and 282,000 are hospitalized; of those hospitalized, 20% will die.
• At least 5.3 million Americans - 2% of the US population - live with disabilities from TBI.
• Men are twice as likely to sustain a TBI.
• Most common causes: falls and motor vehicle accidents. Others: firearms, assaults, sports-related trauma, recreational injuries, war-related injuries.

Three time points of death after head trauma

6.2 Scalp Lacerations

The most easily recognized external head trauma. The scalp contains many blood vessels with poor constrictive abilities, so most scalp lacerations bleed profusely - even relatively small wounds bleed significantly. The major complications are blood loss and infection.

6.3 Skull Fractures

Skull fractures are described three ways: (1) linear or depressed, (2) simple, comminuted, or compound, and (3) closed or open, depending on whether there is a scalp laceration or extension of the fracture into the air sinuses or dura. Type and severity depend on the velocity, momentum, direction, and shape of the injuring agent and the site of impact.

Major complications of skull fractures: intracranial infections, hematoma, and meningeal and brain tissue damage. Treatment is usually conservative; for depressed fractures and fractures with loose fragments, a craniotomy is done to elevate the depressed bone and remove free fragments. If large amounts of bone are destroyed, a craniectomy is done and a cranioplasty will be needed later.

6.4 Manifestations by Fracture Location

Location determines manifestations. Learn this table as a reverse lookup: a question gives you the finding and asks where the fracture is.

Basilar skull fracture is a special type of linear fracture involving the base of the skull. Its manifestations evolve over several hours and include cranial nerve deficits, Battle sign (postauricular bruising), and periorbital bruising (raccoon eyes). It is often the result of a tear in the dura with subsequent leakage of CSF.

6.5 Testing for a CSF Leak

A CSF leak - rhinorrhea from the nose, otorrhea from the ear - confirms that the fracture has traversed the dura. Rhinorrhea may also present as postnasal sinus drainage and may be overlooked unless you assess for it. There are two bedside tests.

Note the color, appearance, and amount of leaking fluid - both tests can give false-positive results.

6.6 Classifying Brain Injury

Severity is classified by the Glasgow Coma Scale: minor = GCS 13 to 15 - moderate = GCS 9 to 12 - severe = GCS 3 to 8.

6.7 Concussion

A concussion is a sudden, transient mechanical head injury with disruption of neural activity and a change in level of consciousness. It is a minor diffuse head injury.

• Typical signs: brief disruption in LOC, amnesia about the event (retrograde amnesia), and headache. The patient may or may not lose total consciousness.
• Manifestations are usually short in duration and resolve spontaneously; concussion is usually considered benign.
• For some patients the signs are the beginning of a more serious, progressive problem - especially with a history of concussion or head injury.
• Discharge rule: if the patient has NOT lost consciousness, or loss of consciousness lasted LESS THAN 5 MINUTES, the patient is usually discharged with instructions to notify the provider if symptoms persist or behavior changes occur. Give patient and caregiver instructions for observation and accurate reporting.

Home teaching for the first 2 to 3 days after head injury

Notify the health care provider immediately for any of the following, which may indicate complications:

• Increased drowsiness - difficulty arousing, confusion
• Nausea or vomiting
• Worsening headache or stiff neck
• Seizures
• Vision changes (blurring) or sensitivity to light
• Behavior changes - irritability, anger
• Motor problems - clumsiness, difficulty walking, slurred speech, weakness in arms or legs
• Sensory problems - numbness
• Heart rate below 60 beats/min

Also: have someone stay with you; abstain from alcohol; check with the provider before taking any drug that may increase drowsiness - muscle relaxants, tranquilizers, opioid analgesia; and avoid driving, heavy machinery, contact sports, and hot baths.

6.8 Diffuse Axonal Injury

Diffuse axonal injury (DAI) is widespread axonal damage occurring after mild, moderate, or severe TBI. It is located primarily around axons in the subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus, and brainstem.

• Clinical signs vary: decreased LOC, increased ICP, decortication or decerebration, global cerebral edema.
• Survivors of the initial event are admitted to the ICU and vigilantly watched for signs of increased ICP.
• Severe injury carries a poor functional prognosis.

6.9 Focal Injury - Contusion and Laceration

A contusion is bruising of the brain tissue within a focal area. It is usually associated with a closed head injury and often occurs at a fracture site. There may be areas of bleeding, infarction, necrosis, and edema.

Coup-contrecoup injury

Damage occurs when the brain moves inside the skull under a high-energy, high-impact mechanism.

• Coup - contusion or laceration at the site of direct impact of brain on skull.
• Contrecoup - a second area of damage on the OPPOSITE side, away from the point of injury, as the brain rebounds.
• The result is multiple contused areas, and contrecoup injuries tend to be MORE SEVERE.
• Overall prognosis depends on the amount of bleeding around the contusion site.
• Neurologic assessment may show focal and generalized manifestations, depending on the contusion's size and location.
• Seizures can occur, especially with frontal or temporal lobe involvement.

Lacerations

A laceration is actual tearing of brain tissue, occurring most often in depressed and open fractures and penetrating injuries. Tissue damage is severe, and surgical repair of the laceration is impossible because of the nature of brain tissue. Management is antibiotics until meningitis is ruled out plus preventing secondary injury from increased ICP. If bleeding is deep into brain tissue, both focal and generalized signs develop.

Intracerebral hemorrhage generally follows a cerebral laceration and manifests as a space-occupying lesion with unconsciousness, hemiplegia on the CONTRALATERAL side, and a dilated pupil on the IPSILATERAL side. As the hematoma expands, signs of increased ICP become more severe. Subarachnoid and intraventricular hemorrhage can also occur from head trauma. The delayed responses to major head trauma are bleeding, hematoma formation, seizures, and cerebral edema.

6.10 Emergency Management of Head Injury

6.11 Diagnostics and Nursing Care in Head Injury

• CT is the BEST test to evaluate head trauma - it allows rapid diagnosis and intervention in the acute setting.
• MRI is MORE SENSITIVE than CT in detecting SMALL lesions. PET and evoked potential studies may also be used.
• Transcranial Doppler can measure CBF velocity.

A patient with a head injury always has the potential to develop increased ICP, which carries higher mortality and poorer functional outcomes. The general nursing goal is to maintain cerebral oxygenation and perfusion and prevent secondary cerebral ischemia. Surveillance for changes in neurologic status is critically important, because the patient's condition may deteriorate rapidly and require emergency surgery. Report any sign of a deteriorating neurologic state, no matter how subtle - a small drop in LOC or in motor strength - to the provider.

Specific problems needing intervention

If the patient's condition deteriorates, they may need a burr-hole opening or craniotomy. The emergency nature of the surgery may hasten the usual preoperative preparation. The patient is often unconscious before surgery, so a family member must sign the consent form - which requires sensitive nursing management and a team approach that includes social work.

6.12 Long-Term Consequences and Family Teaching

• Seizure disorders may occur even in nonpenetrating head injury. Seizures may develop during the first week after injury or not until years later. Prophylactic antiseizure drugs for posttraumatic seizures are a controversial practice.
• Mental and emotional sequelae are often the MOST INCAPACITATING problems. One consequence of TBI is that the person may not realize a brain injury has occurred.
• Patients comatose for more than 6 hours may have some personality change. Expect loss of concentration and memory, defective memory processing, decreased personal drive, increased apathy, euphoria and mood swings, apparent lack of awareness of the seriousness of the injury, and loss of social restraint, judgment, tact, and emotional control.
• Progressive recovery may continue for YEARS. Return to work and staying employed are real challenges.
• The patient's outward physical appearance does NOT necessarily reflect what has happened in the brain and is not a good indicator of ultimate function at home or at work.

Expected outcomes. The patient will maintain normal CPP, achieve maximal cognitive, motor, and sensory function, and have no infection or fever.

7.1 Where the Blood Is

Three hematomas, three anatomic planes, and the plane determines the vessel, which determines the speed, which determines the presentation. Work outward from the skull:

7.2 Epidural Hematoma - a Neurologic Emergency

An epidural hematoma is usually caused by a linear fracture crossing a major artery in the dura, tearing it. Because the temporal bone is thin and the middle meningeal artery runs beneath it, a temporal fracture is the classic setup.

7.3 Subdural Hematoma

A subdural hematoma usually results from injury to the brain tissue and its blood vessels. Most arise from the veins that drain from the surface of the brain into the sagittal sinus, which is why they are usually venous and usually slower - and why they are classified by how long they take to declare themselves.

• Acute. Manifests within hours; signs resemble brain tissue compression in increased ICP - decreasing LOC and headache. Size determines presentation and prognosis; appearance ranges from drowsy and confused to unconscious. The IPSILATERAL pupil dilates and becomes fixed if ICP is significantly increased. Blunt-force injuries producing acute subdural hematomas may cause significant underlying brain injury → cerebral edema → increased ICP → increased morbidity and mortality despite surgical evacuation.
• Subacute. Usually 2 to 14 days after injury. After the initial bleed, the hematoma may appear to ENLARGE over time as the breakdown products of blood draw fluid into the subdural space - an osmotic mechanism, not new bleeding.

7.4 Chronic Subdural Hematoma in the Older Adult

This is the single most testable hematoma scenario in the chapter, because everything about it is counterintuitive.

• It develops weeks to months after a seemingly minor head injury.
• It is more common in older adults because brain atrophy creates a potentially larger subdural space. With atrophy the brain stays attached to its supportive structures, so tension increases and the bridging veins become subject to tearing.
• Because the subdural space is larger, the presenting problem is FOCAL SYMPTOMS rather than signs of increased ICP - there is room for the blood before pressure rises.
• Patients with a history of alcohol use are prone to subdural hematomas because of an increased incidence of falls.
• Diagnosis may be DELAYED in older adults because symptoms - confusion, lethargy, memory loss - mimic other problems and are often attributed to vascular disease (stroke, TIA) or dementia.

7.5 Intracerebral Hematoma

Bleeding within the brain tissue, occurring in about 16% of head injuries. It is usually located in the frontal and temporal lobes, possibly from rupture of intracerebral vessels at the time of injury. The SIZE and LOCATION of the hematoma are the key determinants of outcome. It presents as a space-occupying lesion: unconsciousness, contralateral hemiplegia, and an ipsilateral dilated pupil.

7.6 Surgical Management of Hematomas

• Large acute subdural and epidural hematomas, or those with significant neurologic impairment, require surgical evacuation. A craniotomy is usually done so the surgeon can see and control the bleeding vessels.
• Burr-hole openings may be used in an extreme emergency for more rapid decompression, followed by a craniotomy.
• A drain may be placed after surgery for several days to prevent blood from reaccumulating.
• When extreme swelling is expected - as with DAI or ongoing bleeding - a CRANIECTOMY may be done, removing a piece of skull to reduce pressure inside the head and reduce the risk for herniation.

8.1 Types of Cranial Surgery

Indications include brain tumors, CNS infection such as an abscess, vascular abnormalities, craniocerebral trauma, seizure disorder, and intractable pain.

In a craniotomy, the surgeon drills a set of burr holes, connects them with a saw, and removes the bone flap. Afterward the bone flap is secured with small plates or wired shut, and drains may be placed to remove fluid and blood. Patients usually receive care in the ICU until stable.

8.2 Nursing Care After Cranial Surgery

The main goal of care after cranial surgery is preventing increased ICP. Frequent assessment of neurologic status is essential during the first 48 hours.

• Closely monitor fluid and electrolyte levels and serum osmolality to detect changes in sodium regulation, the onset of diabetes insipidus, or severe hypovolemia.
• Monitor for pain and nausea. Nausea and vomiting are common after surgery; give antiemetics as ordered - but do NOT give promethazine: it can increase somnolence and change the accuracy of a neurologic assessment.
• Although the brain has no pain receptors, patients often report headache caused by edema or by pain at the incision site. Control pain with SHORT-ACTING OPIOIDS and monitor neurologic status.

• Observe the dressing for color, odor, and amount of drainage. Notify the provider immediately of any excess bleeding or clear drainage - clear drainage suggests a CSF leak.
• Check drains for placement and assess the area around the dressing.
• Meticulous scalp and incision care prevents wound infection. Once the dressing is off, use an antiseptic soap for washing the scalp. Explain preoperatively that some hair may be shaved, usually in the operating room after induction of anesthesia; the psychologic impact can be lessened with a wig, turban, scarf, or cap. For a patient receiving radiation, teach the use of sunblock and a head covering.
• Rehabilitation potential cannot be determined until cerebral edema and increased ICP subside postoperatively. Maintain function through careful positioning, meticulous skin and mouth care, regular range of motion, bowel and bladder care, and adequate nutrition; collaborate with physical therapy, speech therapy, and social work.
• Cognitive and emotional residual deficits are often harder for families to accept than motor and sensory losses.

8.3 Inflammatory Conditions of the Brain - Overview

Brain abscess, meningitis, and encephalitis are the most common inflammatory conditions of the brain and spinal cord. Causes include bacteria, viruses, fungi, and chemicals - contrast media used in diagnostic tests, or blood in the subarachnoid space. CNS infections may enter via the bloodstream, by extension from a primary site, or along cranial and spinal nerves. Mortality is about 10% to 15% in the general population and higher in older and immunosuppressed patients. Some who recover have long-term neurologic deficits, including hearing loss.

8.4 Bacterial Meningitis - Etiology and Pathophysiology

Bacterial meningitis is an acute inflammation of the meningeal tissues surrounding the brain and spinal cord. It usually occurs in fall, winter, or early spring and is often related to a viral respiratory disease. Older adults and debilitated persons are affected more often, and college students living in dormitories and people living in institutions such as prisons carry a high risk. Untreated bacterial meningitis has a high mortality rate.

• Streptococcus pneumoniae and Neisseria meningitidis are the leading causes.
• N. meningitidis has at least 13 serogroups; 5 (A, B, C, Y, W) cause most cases.
• Haemophilus influenzae was once the most common cause; the H. influenzae vaccine has significantly decreased meningitis from this organism.
• Organisms usually enter the CNS through the upper respiratory tract or the bloodstream, and may also enter by direct extension from penetrating skull wounds or through fractured sinuses in basilar skull fractures.

8.5 Clinical Manifestations

• Key signs: fever, severe headache, nausea, vomiting, and NUCHAL RIGIDITY (neck stiffness).
• Photophobia, decreased LOC, and signs of increased ICP may be present.
• The headache becomes progressively worse and may be accompanied by vomiting and irritability.
• Coma is associated with a POOR PROGNOSIS and occurs in 5% to 10% of patients with bacterial meningitis.
• Seizures occur in ONE THIRD of all cases.
• If the organism is meningococcus, a SKIN RASH is common. Petechiae may be seen on the trunk, lower extremities, and mucous membranes.

8.6 Complications

• The most common acute complication is INCREASED ICP. Most patients have it, and it is the major cause of an altered mental status.
• Acute cerebral edema may cause seizures, CN III palsy, bradycardia, hypertensive coma, and death.
• Headaches may occur for MONTHS after diagnosis, until the irritation and inflammation completely resolve. Implement pain management for the chronic headache.
• Noncommunicating hydrocephalus may occur if exudate causes adhesions that prevent normal CSF flow from the ventricles, or if CSF reabsorption by the arachnoid villi is obstructed by exudate. Surgical implantation of a shunt is the only treatment.
• Hemiparesis, dysphasia, and hemianopsia may occur and usually resolve. If they do NOT resolve, suspect a cerebral abscess, subdural empyema, subdural effusion, or persistent meningitis.

Cranial nerve involvement

8.7 Diagnostic Studies and CSF Analysis

• With manifestations suggestive of bacterial meningitis, do a blood culture and a CT scan.
• Diagnosis is usually verified by LUMBAR PUNCTURE with CSF analysis.
• Safety: the LP should be done ONLY AFTER the CT scan has ruled out an obstruction in the foramen magnum - to prevent a fluid shift resulting in herniation.
• Specimens of CSF, sputum, and nasopharyngeal secretions are taken for culture BEFORE antibiotic therapy starts. A Gram stain detects bacteria.
• The predominant WBC type in CSF with bacterial meningitis is NEUTROPHILS.
• Skull x-rays may show infected sinuses. CT and MRI may be NORMAL in uncomplicated meningitis; in other cases CT may show increased ICP or hydrocephalus.

8.8 Interprofessional and Nursing Care of Meningitis

Other drug therapy: codeine for headache, acetaminophen or aspirin for a temperature above 100.4°F (38°C), IV phenytoin for seizures, and IV mannitol for diuresis. Management otherwise is rest, IV fluid, and hypothermia.

Acute nursing care

• Assess vital signs, neurologic status, intake and output, skin, and lung sounds at regular intervals based on the patient's condition.
• Administer antibiotics AS SCHEDULED to maintain therapeutic blood levels.
• Pain and comfort: codeine provides pain relief without undue sedation for most patients. Assist the patient to a position of comfort - often curled up with the head slightly extended - and elevate the head of the bed slightly. A darkened room and a cool cloth over the eyes relieve photophobia.
• All patients have some degree of mental distortion and hypersensitivity and may misinterpret the environment. Minimize environmental stimuli and prevent injury. For the patient with delirium, low lighting may decrease hallucinations. A familiar person at the bedside can have a calming effect. Be efficient with care while conveying unhurried gentleness; use touch, a soothing voice, and simple explanations.
• If seizures occur, assess the patient, take protective measures, and give antiseizure drugs - phenytoin or levetiracetam (Keppra) - as ordered.

Fluids. High fever increases metabolic rate and insensible fluid loss, so assess for dehydration and adequacy of intake; diaphoresis further increases fluid losses and should be noted on the output record. The chapter gives a replacement calculation: 800 mL/day for respiratory losses plus 100 mL for each degree of temperature greater than 100.4°F (38°C). Supplemental enteral feeding may be needed to maintain nutrition.

Recovery and residual effects

• After the acute period the patient needs several weeks of recovery before resuming normal activities. Stress adequate nutrition: a high-protein, high-calorie diet in small, frequent feedings.
• Muscle rigidity may persist in the neck and the backs of the legs - progressive range of motion exercises and warm baths are useful. Increase activity gradually, with adequate rest and sleep.
• Residual sequelae: dementia, seizures, deafness, hemiplegia, and hydrocephalus. Assess vision, hearing, cognitive skills, and motor and sensory abilities after recovery and provide referrals as needed.

Expected outcomes. The patient will have appropriate cognitive function, maintain body temperature within normal range, and report satisfaction with pain control.

8.9 Viral Meningitis, Brain Abscess, and Encephalitis

9.1 Kidney Failure, and the Two Ways It Arrives

Kidney failure is classified as acute or chronic. Acute kidney injury (AKI) has a rapid onset. Chronic kidney disease (CKD) is gradual, with a progressive decline in kidney function. The chapter opens with a comparison table because the two diseases share a final common picture - retained waste, retained fluid, retained potassium - while differing in almost everything that matters for care.

9.2 What AKI Is - Rapid Loss, With or Without Oliguria

AKI is the term that encompasses the entire scope of the syndrome, ranging from a slight deterioration in kidney function to severe impairment. It is characterized by a rapid loss of kidney function with or without decreased urine output. Hold on to the second half of that phrase. A student who has learned that kidney failure means the urine stops will miss half the patients on the unit.

The loss of function is accompanied by progressive increases in blood urea nitrogen (BUN), creatinine, and potassium. The severity can range from a small increase in serum creatinine or a reduction in urine output all the way to azotemia - an accumulation of nitrogenous waste products, meaning urea nitrogen and creatinine, in the blood. Azotemia is a laboratory finding, a number on a chemistry panel. It is not the same as uremia, which is the multisystem syndrome the CKD half of the chapter describes and which is covered in Unit 11.

• AKI can develop over hours or days.
• Although AKI is potentially reversible, it carries a high mortality rate.
• AKI usually affects people who already have other life-threatening problems. It often follows severe prolonged hypotension, hypovolemia, or exposure to a nephrotoxic agent.
• Hospitalized patients develop AKI at a high rate - 1 in 5 - and have a high mortality rate.
• When AKI develops in an ICU patient, the mortality rate can be as high as 80%.

9.3 Prerenal Causes - Perfusion Failure Without Tissue Damage

The causes of AKI are categorized as prerenal, intrarenal (or intrinsic), and postrenal. Prerenal causes are factors that reduce systemic circulation, causing decreased renal blood flow. The decrease in blood flow leads to decreased glomerular perfusion and filtration of the kidneys. Nothing is wrong with the kidney itself. The kidney is a filter that has been starved of the pressure it needs to filter.

The mechanism in full: with a decrease in circulating blood volume, autoregulatory mechanisms that increase angiotensin II, aldosterone, norepinephrine, and antidiuretic hormone try to preserve blood flow to essential organs. Every one of those four hormones does the same two things - hold on to sodium and hold on to water - and the urine chemistry shows it. Prerenal azotemia results in decreased sodium excretion (less than 20 mEq/L), increased sodium and water retention, and decreased urine output.

The bridge between the categories is the sentence students most often skip: prerenal problems can contribute to intrarenal AKI. If decreased perfusion persists for an extended time, the kidneys lose their ability to compensate and damage to kidney tissue occurs. Prerenal is a reversible state with an expiration date. Left uncorrected it converts into the intrarenal disease described next, and at that point the reversibility of the first category is gone.

9.4 Intrarenal Causes and Acute Tubular Necrosis

Intrarenal causes include problems that cause direct damage to the kidney tissue, resulting in impaired nephron function. The damage usually results from prolonged ischemia, nephrotoxins (for example aminoglycosides and contrast media), hemoglobin released from hemolyzed red blood cells, or myoglobin released from necrotic muscle cells.

The mechanisms are physical as much as chemical. Nephrotoxins can cause obstruction of intrarenal structures by crystallizing, or can damage the epithelial cells of the tubules. Hemoglobin and myoglobin can block the tubules and cause renal vasoconstriction. That is the reason a crush injury is a kidney emergency: the myoglobin dumped out of necrotic muscle both plugs the tubules mechanically and constricts the vessels supplying them, so the tubule is simultaneously obstructed and starved. Kidney diseases such as acute glomerulonephritis and systemic lupus erythematosus can also cause AKI.

Acute tubular necrosis

• Acute tubular necrosis (ATN) is the most common intrarenal cause of AKI in hospitalized patients.
• It can result from ischemia, nephrotoxins, or sepsis.
• Ischemic and nephrotoxic ATN together cause 90% of intrarenal AKI cases.
• Other in-hospital risk factors for ATN: major surgery, shock, blood transfusion reaction, muscle injury from trauma, and prolonged hypotension.

9.5 Postrenal Causes - Obstruction and the 48-Hour Window

Postrenal causes involve mechanical obstruction in the outflow of urine. With the flow of urine obstructed, urine refluxes into the renal pelvis, impairing kidney function. The most common postrenal causes are benign prostatic hyperplasia, prostate cancer, stones, trauma, and extrarenal tumors.

The mechanism is a pressure problem working backwards up the tract: bilateral ureteral obstruction leads to hydronephrosis (kidney dilation), an increase in hydrostatic pressure, and tubular blockage, resulting in a progressive decline in kidney function. Filtration at the glomerulus depends on a pressure gradient; raise the pressure on the downstream side high enough and filtration stops even though the glomerulus itself is untouched.

• If bilateral obstruction is relieved within 48 hours of onset, complete recovery is likely.
• Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis.
• Postrenal causes account for less than 10% of AKI cases.

9.6 The Full Cause List (Table 51.2)

The chapter's cause table is worth reading as three lists organized by the same anatomic logic. In the prerenal column every entry is a way of lowering renal blood flow - by pump failure, by vasodilation, by blocking the renal vessels, or by emptying the tank. In the intrarenal column every entry is a way of injuring nephron tissue directly. In the postrenal column every entry is a physical blockage.

9.7 Staging AKI - The RIFLE Classification

This chapter stages AKI by RIFLE and by RIFLE only. The acronym is built from five terms: Risk, Injury, Failure, Loss, and End-stage renal disease. The chapter states the structure explicitly: Risk is the first stage of AKI, followed by Injury as the second stage, then AKI increases in severity to the last or third stage, Failure. The two outcome variables are Loss and End-stage renal disease. Three stages of severity, then two outcomes. Loss and ESRD are not severities of AKI; they are what happens when AKI does not resolve.

Two independent criteria define each of the first three stages, and a patient needs only one of them. One criterion is a filtration criterion, read from serum creatinine or calculated GFR. The other is a urine output criterion, read in mL/kg/hr over a stated number of hours. This matters clinically because roughly half of AKI patients are nonoliguric, and in those patients the creatinine criterion is the only one that will stage them.

9.8 Where the Chapter Contradicts Itself, and What It Leaves Out

Two disagreements inside these pages are the kind that generate ambiguous question stems, and one absence will surprise anyone who has seen AKI staged elsewhere. Neither is resolved silently here.

10.1 Oliguric Phase - Urine Output and Urinalysis

• The most common initial manifestation of AKI is oliguria, a reduction in urine output to less than 400 mL/day, usually within 1 to 7 days of the injury.
• If the cause is ischemia, oliguria often occurs within 24 hours. When nephrotoxic drugs are involved, the onset may be delayed for as long as 1 week.
• The phase lasts on average 10 to 14 days and can last months. The longer the oliguric phase lasts, the poorer the prognosis for complete recovery.
• Nonoliguric AKI has a urine output greater than 400 mL/day, and about 50% of patients will be nonoliguric, making initial diagnosis harder.
• The pattern points to the cause: anuria is usually seen with urinary tract obstruction; oliguria often occurs with prerenal causes; nonoliguric AKI occurs with acute interstitial nephritis and ATN.

A urinalysis may show casts, red blood cells, and white blood cells. The casts are the most instructive: they form from mucoprotein impressions of the necrotic renal tubular epithelial cells, which slough into the tubules. A cast is a mould of the tubule lumen - physical evidence that tubular epithelium has died and come loose. Proteinuria may be present if AKI is related to glomerular membrane dysfunction.

10.2 Oliguric Phase - Fluid, Acidosis, and Sodium

Hypovolemia has the potential to worsen all forms of AKI, and fluid replacement alone often treats prerenal causes. But once urine output falls, fluid retention occurs: the neck veins may become distended with a bounding pulse, edema and hypertension may develop, and fluid overload can eventually lead to heart failure, pulmonary edema, and pericardial and pleural effusions.

The metabolic acidosis has a two-part mechanism. Impaired kidneys cannot excrete hydrogen ions or the acid products of metabolism. Serum bicarbonate production decreases from defective reabsorption and regeneration of bicarbonate ions, and the bicarbonate that remains is depleted through buffering of acidic hydrogen ions and metabolic end products. The kidney stops removing acid and stops making base, so the measured bicarbonate falls from both ends. The patient with severe acidosis may develop rapid, deep respirations to try to compensate by increasing carbon dioxide exhalation - the only compensation left.

For sodium, damaged tubules cannot conserve sodium. Urinary sodium excretion may increase, resulting in normal or below-normal levels of serum sodium - the mirror image of the prerenal picture in Unit 9. Excess sodium intake is still avoided, because it can lead to volume expansion, hypertension, and heart failure, and the water side matters too: uncontrolled hyponatremia or water excess can lead to cerebral edema.

10.3 Oliguric Phase - Hyperkalemia

The kidneys normally excrete 80% to 90% of the body's potassium, so in AKI the serum potassium level increases because the kidney's normal ability to excrete potassium is impaired. Three mechanisms then add potassium on top of the retention.

• Massive tissue trauma raises the risk sharply because damaged cells release potassium into the extracellular fluid - potassium is overwhelmingly intracellular, so anything that breaks cells open dumps it into plasma. Bleeding and blood transfusions may cause cellular destruction, releasing more.
• Metabolic acidosis worsens hyperkalemia as hydrogen ions enter the cells and potassium is driven out into the ECF. The acidosis of section 10.2 is one of the causes of the hyperkalemia, not a separate problem.
• While patients with hyperkalemia are often asymptomatic, some may have weakness with severe hyperkalemia - which is why potassium is followed by laboratory value and ECG, not by how the patient looks.

The chapter names the ECG changes: acute or rapid development of hyperkalemia may produce peaked T waves, widening of the QRS complex, and ST segment depression, and because cardiac muscle is intolerant of acute increases in potassium, emergency treatment of hyperkalemia is needed.

10.4 Oliguric Phase - Waste Products, Blood, and Brain

The kidneys are the main excretory organs for urea, an end product of protein metabolism, and creatinine, an end product of endogenous muscle metabolism, and both rise in kidney disease. They are not equally trustworthy. An increased BUN can also be caused by dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury, or GI bleeding. The best serum indicator of AKI is creatinine because it is not affected by other factors.

Hematologically, hospital-acquired AKI often occurs in patients who have multiorgan failure, and leukocytosis is often present. Then the sentence that should reorganize nursing priorities: the most common cause of death in AKI is infection, and the most common sites are the urinary and respiratory systems. Every aseptic-technique instruction later in this unit descends from it. Neurologically, changes occur as the nitrogenous waste products accumulate in the brain and other nervous tissue, and manifestations can be as mild as fatigue and difficulty concentrating and escalate to seizures, stupor, and coma - a graded scale, which is why level of consciousness is on the daily assessment list.

10.5 The Diuretic and Recovery Phases

The turn from oliguria to diuresis feels like recovery and is not, yet. Daily urine output is usually around 1 to 3 L and may reach 5 L or more, but the nephrons are still not fully functional even as urine output increases. The mechanism: the high urine volume is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and the inability of the tubules to concentrate the urine. In this phase, the kidneys have recovered their ability to excrete wastes but not to concentrate the urine.

• Hypovolemia and hypotension can occur from massive fluid losses - the danger has flipped from overload to depletion - and large losses of fluid and electrolytes require monitoring for hyponatremia, hypokalemia, and dehydration.
• The diuretic phase may last 1 to 3 weeks, and near the end of it the acid-base, electrolyte, and waste product values stabilize.
• The recovery phase begins when the GFR increases, allowing BUN and creatinine to decrease. Major improvements occur in the first 1 to 2 weeks, but it may take 12 months for kidney function to stabilize.
• Some patients do not recover and progress to ESRD, the older adult is less likely to have a complete recovery, and patients who recover may achieve clinically normal kidney function but remain in an early stage of CKD.

10.6 Diagnostic Studies

The history is essential for diagnosing the cause of AKI, and it maps onto the three categories of Unit 9: prerenal with a history of dehydration, hypotension, or blood loss; intrarenal after exposure to nephrotoxic drugs or contrast media; postrenal with a history of changes in the urinary stream, stones, BPH, or bladder or prostate cancer.

10.7 Interprofessional Care - Fluid, Potassium, and Dialysis

Because AKI is potentially reversible, the main goals are to eliminate the cause, manage the signs and symptoms, and prevent complications while the kidneys recover. The first step is to determine whether there is adequate intravascular volume and cardiac output to ensure adequate kidney perfusion - the prerenal question, because it is the one fluid alone can fix. Diuretic therapy may be given, usually loop diuretics such as furosemide or bumetanide, or an osmotic diuretic such as mannitol.

Hyperkalemia is one of the most serious complications in AKI because it can cause life-threatening dysrhythmias. The chapter groups the therapies by what they accomplish: insulin and sodium bicarbonate are temporary measures that promote a transient shift of potassium into the cells, and potassium will eventually diffuse back into the bloodstream; calcium gluconate raises the threshold at which dysrhythmias occur, temporarily stabilizing the myocardium; sodium polystyrene sulfonate and dialysis remove potassium from the body.

Conservative therapy may be all that is necessary until kidney function improves; if it is not effective, renal replacement therapy is used, and controversy exists about the timing of RRT in AKI. The six most common indications: volume overload compromising cardiac or pulmonary status; high serum potassium; metabolic acidosis with serum bicarbonate less than 15 mEq/L; BUN greater than 120 mg/dL; significant change in mental status; and pericarditis, pericardial effusion, or cardiac tamponade.

There is no consensus about the best RRT approach.Peritoneal dialysis is a viable option but is not often used. Intermittent hemodialysis and CRRT have both been used effectively.CRRT is provided continuously over 24 hours through cannulation of a vein or catheter placement and has much slower blood flow rates than intermittent HD. Hemodialysis is the method of choice when changes are needed emergently, though it is technically more complicated, requires anticoagulation to prevent clotting when blood contacts the dialysis circuit, and rapid fluid shifts during HD may cause hypotension. The mechanics belong to the CKD half of the chapter and are covered in Unit 13.

10.8 Nutrition Therapy in AKI

The goal is to provide adequate calories to prevent catabolism despite restrictions that prevent electrolyte and fluid problems and azotemia. A starving patient breaks down their own muscle, and that produces exactly the two things the failing kidney cannot handle: nitrogenous waste and potassium. Feeding the patient protects the kidney's workload.

• 30 to 35 kcal/kg and 0.8 to 1.0 g of protein per kg of desired body weight, to prevent the breakdown of body protein.
• Adequate energy should mainly come from carbohydrate and fat sources, to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. Fat is increased so the patient receives at least 30% to 40% of total calories from fat, and IV fat emulsion infusions provide a good source of nonprotein calories.
• Essential amino acids may be supplemented. Potassium and sodium are regulated per plasma levels, and sodium is restricted as needed to prevent edema, hypertension, and heart failure.
• If oral intake cannot be maintained, enteral nutrition is the preferred route; when the GI tract is not functional, parenteral nutrition can provide adequate nutrition, though the patient treated with PN may need daily hemodialysis or CRRT to remove the excess fluid.

10.9 Nursing Management - Assessment, Prevention, and Acute Care

Daily weights, strict intake and output, and vital signs are key, and daily monitoring of urine output has prognostic value; it is crucial for determining therapy and daily fluid volume replacement. The rest of the assessment is a system-by-system search for the complications above: urine color, specific gravity, glucose, protein, blood, and sediment; edema, neck vein distention, bruises; a dialysis access site for inflammation and exudate; mental status and level of consciousness; oral mucosa for dryness and inflammation; lungs for crackles, wheezes, or decreased breath sounds; the heart for an S3 gallop, murmurs, or a pericardial friction rub; and ECG readings for dysrhythmias. The four clinical problems are electrolyte imbalance, fluid imbalance, risk for infection, and anxiety.

Prevention and early recognition of AKI are the most important aspects of care, directed toward identifying and monitoring high-risk populations, controlling exposure to nephrotoxic drugs and industrial chemicals, and preventing prolonged episodes of hypotension and hypovolemia. In hospital, the risk factors are preexisting CKD, older age, massive trauma, major surgery, extensive burns, heart failure, sepsis, and obstetric complications.

• Assess and record extrarenal losses from vomiting, diarrhea, hemorrhage, and increased insensible losses; prompt replacement of significant fluid losses helps prevent ischemic tubular damage. Note that aggressive diuretic therapy for fluid overload from any cause can lead to decreased renal blood flow - the treatment for one problem is a cause of another.
• Monitor kidney function in persons taking potentially nephrotoxic drugs, which should be used sparingly in high-risk patients, in the smallest effective doses, for the shortest possible periods, and caution the patient about OTC analgesics, especially NSAIDs. ACE inhibitors can decrease perfusion pressure and cause hyperkalemia and may have to be reduced or stopped - but they are often used to prevent proteinuria and progression of kidney disease, especially in patients with diabetes.
• Take daily weights with the same scale at the same time each day.1 kg is equivalent to 1000 mL of fluid - the most useful conversion in this unit.
• Because infection is the leading cause of death in AKI, meticulous aseptic technique is critical. Watch for local manifestations - swelling, redness, pain - and systemic ones - fever, malaise, leukocytosis. But patients with AKI have a blunted febrile response to infection: waiting for a temperature is waiting for a sign that may never come.
• If antibiotics are given, carefully consider type, frequency, and dosage, because the kidneys are the main route of excretion for many antibiotics.Perform good skin care and prevent pressure injuries, and give mouth care to prevent stomatitis, which develops when ammonia made by bacterial breakdown of urea irritates the mucous membranes.

Recovery from AKI is highly variable, depending on whether other body systems fail, the patient's general health and age, the length of the oliguric phase, and the severity of nephron damage. Protein and potassium intake are dictated by kidney function, and regular evaluation of kidney function is necessary. Teach the signs and symptoms of recurrent kidney disease and measures to prevent recurrence. The long-term convalescence of 3 to 12 months may cause psychosocial and financial hardships, and if the kidneys do not recover, the patient will need to transition to life on chronic dialysis or a possible transplant.

10.10 Gerontologic Considerations in AKI

• The GFR declines with age, so the reserve is lower before anything goes wrong, and impaired function of other organ systems from cardiovascular disease or diabetes can increase the risk.
• The aging kidney is less able to compensate for changes in fluid volume, solute load, and cardiac output - a blunting of the autoregulatory response described in Unit 9.
• Dehydration is a predisposing factor, from polypharmacy - diuretics, laxatives, drugs that suppress appetite or consciousness - acute febrile illness, and immobility. Other causes: hypotension, diuretic therapy, aminoglycoside therapy, obstructive disorders such as BPH, surgery, infection, and contrast media.
• Mortality rates are similar for older and younger patients, but patients over 65 years of age are less likely to recover from AKI. Despite this, age is not a barrier to offering RRT.

11.1 What CKD Is - Definition, Prevalence, and Cause

• CKD involves progressive, irreversible loss of kidney function.More than 26 million American adults - 1 out of every 9 - have CKD, a rise partly attributed to an aging population and increased rates of obesity, diabetes, and hypertension.
• Because the kidneys are highly adaptive, CKD is often not recognized until there has been considerable loss of nephrons, so it is underdiagnosed and untreated and about 70% of people with CKD are unaware that they have the disease.
• Leading causes: diabetes, about 50%, and hypertension, about 25%. Less common: glomerulonephritis, cystic diseases, urologic diseases.
• Over half a million Americans are receiving treatment for ESRD; as the stage progresses the mortality rate increases, and mortality rates are as high as 19% to 24% for patients with ESRD on dialysis. Since 1972 Medicare has covered most dialysis costs, paying 80% of eligible charges, with the state, private insurance, or the patient covering the rest.

11.2 Risk Factors and Who Is Affected

The chapter attaches population figures to the ethnicity row rather than leaving it abstract. Black Americans have the highest rate of CKD, nearly 4 times that of White persons, and are at high risk for CKD as a complication of hypertension. Native Americans have a rate twice that of White persons, and 6 times higher among Native Americans with diabetes than among other ethnic groups with diabetes. The rate in Hispanic persons is 1.5 times higher than in non-Hispanic White persons. Prognosis overall is highly variable: some people live normal, active lives while others progress rapidly to stage 5.

11.3 Staging CKD, Measuring Kidney Function, and Making the Diagnosis

Here the chapter names a formal guideline. Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines defines CKD as either the presence of kidney damage or a decreased GFR less than 60 mL/min/1.73 m2 for longer than 3 months. Note the word or: a patient with documented kidney damage and a normal GFR still has CKD, which is why stages 1 and 2 exist.

Serum creatinine alone poorly reflects kidney function. GFR is the preferred way to determine kidney function. The chapter proves it by running one creatinine value through two different patients.

• Persistent proteinuria is usually the first sign of kidney damage. Screening uses a dipstick for protein, or evaluation for albuminuria, which is not detected with routine urinalysis; patients with diabetes must be checked for albuminuria if routine urinalysis shows no protein.
• The chapter's threshold: a person with persistent proteinuria - 1+ protein on standard dipstick testing 2 or more times over a 3-month period - should have further assessment of risk factors and a diagnostic workup with blood and urine tests.
• Urinalysis detects RBCs, WBCs, protein, casts, and glucose; renal ultrasound detects obstruction and kidney size; a kidney biopsy may be needed to provide a definitive diagnosis. The interprofessional list adds renal scan, CT, BUN, creatinine clearance, serum electrolytes, lipid profile, protein-to-creatinine ratio in the first morning specimen, and hematocrit and hemoglobin.

11.4 Uremia - the Syndrome and Its Map

As kidney function deteriorates, all body systems become affected. The manifestations result from retained urea, creatinine, phenols, hormones, electrolytes, and water. Then the definition: uremia is a syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems. It often occurs when the GFR is 15 mL/min or less. Two qualifiers matter. The manifestations vary depending on the cause, comorbid problems, age, and degree of adherence to the treatment plan, and many patients are tolerant of the changes because they occur gradually - a patient anemic and fatigued for two years does not experience fatigue as new.

One urinary note contradicts the intuition that kidney failure means no urine. In the early stages of CKD, patients usually do not report any change in urine output. Since diabetes is the main cause, polyuria may be present, though not necessarily from the kidney disease. As CKD progresses, patients have increasing difficulty with fluid retention and need diuretic therapy, and after a period on dialysis, patients may develop anuria.

11.5 Metabolic Disturbances and Electrolytes

As the GFR decreases, the BUN and serum creatinine levels increase. The BUN rise reflects protein intake, fever, corticosteroids, and catabolism as well as kidney disease, which is why calculated GFR is a more accurate indicator of kidney function than BUN or creatinine. Significant increases in BUN contribute to nausea, vomiting, lethargy, fatigue, impaired cognition, and headaches - the urea is producing symptoms, not just marking them.

As the GFR decreases, the BUN and serum creatinine levels increase, but the BUN rise also reflects protein intake, fever, corticosteroids, and catabolism, which is why calculated GFR is a more accurate indicator than BUN or creatinine. Significant increases in BUN contribute to nausea, vomiting, lethargy, fatigue, impaired cognition, and headaches - the urea is producing symptoms, not just marking them. Carbohydrate metabolism is disturbed twice over: impaired glucose metabolism from cellular insensitivity to insulin causes defective carbohydrate metabolism with mild to moderate hyperglycemia and hyperinsulinemia, while insulin, which depends on the kidneys for excretion, stays in the circulation longer. The hyperinsulinemia then stimulates hepatic triglyceride production, giving dyslipidemia with increased VLDLs and LDLs and decreased HDLs, related to decreased lipoprotein lipase. Most patients with CKD die from cardiovascular disease.

• Potassium.Fatal dysrhythmias can occur when the serum potassium level reaches 7 to 8 mEq/L - the only numeric potassium threshold printed anywhere in Ch. 51. Hyperkalemia results from the kidneys excreting less potassium, the breakdown of cellular protein, bleeding, and metabolic acidosis, and potassium arrives from foods, diet supplements, drugs, and IV infusions.
• Sodium.Sodium may be high, normal, or low. Impaired excretion means sodium is retained with water, and if large quantities of water are retained, dilutional hyponatremia occurs; retention contributes to edema, hypertension, and heart failure. Sodium intake is patient specific but is often restricted to 2 g/day.
• Magnesium.Magnesium is mainly excreted by the kidneys, and hypermagnesemia is often not a problem unless the patient is ingesting magnesium, giving absent reflexes, decreased mental status, dysrhythmias, and hypotension. Hence the instruction repeated twice more in this guide: do not use magnesium-containing antacids in kidney disease, because the only exit is closed.

11.6 Hematologic System

Normocytic, normochromic anemia is associated with CKD, and the primary cause is decreased erythropoietin production. Erythropoietin normally stimulates precursor cells in the bone marrow to make red blood cells. The kidney is an endocrine organ as well as a filter, and this is the clearest example of what is lost when it fails: the marrow is intact and willing, but no longer receives the signal.

• Other contributors: nutrition deficiencies, decreased RBC life span, increased RBC hemolysis, frequent blood samplings, GI bleeding, and for patients on maintenance hemodialysis blood loss in the dialyzer. Increased parathyroid hormone can inhibit erythropoiesis, shorten RBC survival, and cause bone marrow fibrosis - so the mineral and bone disorder of section 11.9 makes the anemia worse.
• Oral iron supplements may not be effective for the person with CKD - GI side effects hurt adherence, and proton pump inhibitors and phosphate binders decrease absorption; patients on dialysis may need IV iron. Folic acid is dialyzable because it is water soluble, so many patients receive 1 mg/day.
• Bleeding tendencies.The most common cause of bleeding in uremia is a defect in platelet function - impaired aggregation and impaired release of platelet factor III - with increased factor VIII and fibrinogen. Usefully, these can usually be corrected with regular hemodialysis or peritoneal dialysis, because the defect is caused by retained uremic toxins.
• Infection.Both cellular and humoral immune responses are suppressed, with hyperglycemia and external trauma - catheters, needle insertions into vascular access sites contributing: the therapy that keeps the patient alive is a repeated breach of the skin in an immunosuppressed person.

11.7 Cardiovascular, Respiratory, and Gastrointestinal Systems

The most common cause of death in patients with CKD is cardiovascular disease - specifically myocardial infarction, ischemic heart disease, peripheral arterial disease, heart failure, cardiomyopathy, and stroke. The link is close enough that if patients develop cardiac events, kidney function is evaluated. Beyond the traditional risk factors, CKD adds vascular calcification and arterial stiffness: calcium deposits in the vascular medial layer can cause stiffening of the blood vessels, through vascular smooth muscle cells changing into chondrocytes or osteoblast-like cells, high total body calcium and phosphate from abnormal bone metabolism, impaired renal excretion, and the drug therapies used to treat the bone disease.

• Hypertension is both a cause and a consequence of CKD, worsened by sodium retention and increased extracellular fluid volume and sometimes increased renin production. Long-standing hypertension, ECF volume overload, and anemia contribute to left ventricular hypertrophy, leading to cardiomyopathy and heart failure, and hypertension also causes retinopathy, encephalopathy, and nephropathy. BP control is one of the most important therapeutic goals in CKD management.
• Patients are susceptible to dysrhythmias from hyperkalemia and decreased coronary artery perfusion. Uremic pericarditis can progress to pericardial effusion and cardiac tamponade and presents with a friction rub, chest pain, and low-grade fever - which is why the AKI assessment asks you to listen for a rub and why pericarditis is an indication for urgent dialysis.
• Respiratory. Severe acidosis may bring Kussmaul breathing, and dyspnea may come from fluid overload, pulmonary edema, uremic pleuritis, pleural effusions, and pneumonia.

• Gastrointestinal.Stomatitis, a metallic taste, periodontal disease, and uremic fetor - a urinous odor of the breath - often occur, with anorexia, nausea, vomiting, weight loss and malnutrition as ESRD approaches. GI bleeding is a risk because of mucosal irritation and the platelet defect, and constipation follows iron salts or calcium-containing phosphate binders plus the fluid limits and inactivity the treatment plan imposes.

11.8 Neurologic System, Skin, Reproductive System, and Psychologic Changes

Neurologic changes result from increased nitrogenous waste products, electrolyte imbalances, metabolic acidosis, and atrophy and demyelination of nerve fibers - partly reversible chemistry, partly structural nerve damage, which is why the outcomes differ.

• The CNS becomes depressed, producing lethargy, apathy, decreased concentration, fatigue, irritability, and altered mental ability; seizures and coma may result from a rapidly increasing BUN and hypertensive encephalopathy.
• Peripheral neuropathy begins as slowed conduction with paresthesias in the feet and legs as a burning sensation and may progress to bilateral foot drop, muscular weakness and atrophy, and loss of deep tendon reflexes, with muscle twitching, asterixis (a hand-flapping tremor), nighttime leg cramps, and in advanced stage 5, restless legs syndrome. Dialysis should improve general CNS problems and may slow or halt neuropathies, but motor neuropathy may not be reversible.Altered mental status rarely occurs unless the patient has chosen not to have RRT.
• Skin.Refractory itching arises from dry skin, calcium-phosphate deposition in the skin, and sensory neuropathy, is more common in patients receiving dialysis, and may lead to bleeding or infection from scratching. Uremic frost is a rare condition in which urea crystallizes on the skin, usually seen only when BUN levels are very high, for example over 200 mg/dL.
• Reproductive. Both sexes can have infertility and decreased libido; women have anovulation and amenorrhea from low estrogen, progesterone, and luteinizing hormone, and men loss of testicular consistency, decreased testosterone, and low sperm counts. Peripheral neuropathy can cause impotence in men and anorgasmia in women, and sexual function may improve with maintenance dialysis and become normal after a successful transplant.
• Psychologic.Personality and behavioral changes, emotional lability, withdrawal, and depression often occur, compounded by body image changes from edema, skin changes, and access devices. Slowed mental activity can give the appearance of dullness and disinterest in the environment - a caution against reading a uremic patient's flat affect as personality. The patient grieves the loss of kidney function and independence.

11.9 CKD Mineral and Bone Disorder

CKD mineral and bone disorder develops as a systemic disorder of mineral and bone metabolism caused by progressive deterioration in kidney function. It is the chapter's most mechanistic passage and is worth learning as a chain, because each step causes the next and several feed back on earlier ones.

• Skeletal complications are two: osteomalacia, from demineralization with slow bone turnover and defective mineralization of newly formed bone, and osteitis fibrosa, decalcification of the bone and replacement of bone tissue with fibrous tissue.
• Soft tissue complications result from vascular calcifications, a significant contributing factor to cardiovascular disease. Irritation from calcium deposits in the eye can cause uremic red eye, and cardiac calcifications can disrupt the conduction system and cause cardiac arrest.
• The gold standard for diagnosing CKD-MBD is a bone biopsy.

12.1 Goals of Therapy and the Interprofessional Plan

• Early recognition, diagnosis, and treatment can prevent the progression of kidney disease, and patients with CKD need a referral to a nephrologist early in the course of the disease.
• Every effort is made to detect and treat potentially reversible causes - heart failure, dehydration, infections, nephrotoxins, urinary tract obstruction, glomerulonephritis, and renal artery stenosis.
• More patients die from cardiovascular disease than live to need dialysis, so therapy targets CVD plus slowing kidney disease.
• A focus during stages 1 through 4, before the need for dialysis at stage 5, includes controlling blood pressure, hyperparathyroidism, CKD-MBD, anemia, and dyslipidemia.

12.2 Hyperkalemia and Hypertension in CKD

• Management starts with restricting high-potassium foods and drugs. Acute hyperkalemia may need treatment with IV glucose and insulin or IV 10% calcium gluconate - the only concentration printed for any hyperkalemia drug in Ch. 51.
• Sodium polystyrene sulfonate is often given in stage 4 CKD. It has an osmotic laxative action, so tell the patient to expect some diarrhea, and because it exchanges sodium ions for potassium ions, observe for sodium and water retention in a patient already retaining both.
• If changes appear in the ECG, such as peaked T waves and widened QRS complexes, hemodialysis may be done to remove excess potassium.
• Patiromer should not be used in emergency situations because of its delayed onset, and because it binds other oral medications it must be taken at least 6 hours before or after them; sodium zirconium cyclosilicate should be given at least 2 hours apart from other medications.

For some patients, the progression of CKD can be delayed by controlling hypertension. Treatment runs from weight loss, exercise, avoiding alcohol use, and smoking cessation, through the DASH diet, to antihypertensive drugs, with most patients needing 2 or more drugs to reach target BP. ACE inhibitors and ARBs are given to patients with diabetes and those with nondiabetic proteinuria; they decrease proteinuria and may delay the progression of CKD, but must be used with caution, as they can further decrease the GFR and increase serum potassium. Measure the BP supine, sitting, and standing, and teach the patient and caregiver how to monitor BP at home and what readings require immediate intervention.

12.3 CKD-MBD - Phosphate Binders, Vitamin D, and the Parathyroid

The interventions map one to one onto the cascade in section 11.9: limiting phosphorus intake, giving phosphate binders, supplementing vitamin D, and controlling hyperparathyroidism.

• Phosphate intake is not usually restricted until the patient needs RRT. At that time, phosphate is usually limited to about 1 g/day, but diet control alone is usually not enough.
• Calcium-based binders - calcium acetate and calcium carbonate - bind phosphate in the bowel and then excrete it in the stool, but giving calcium increases the calcium load, which increases the risk for vascular calcifications.
• Non-calcium-based binders are used when calcium levels are increased or there is evidence of existing vascular or soft tissue calcifications: lanthanum carbonate (Fosrenol), sevelamer carbonate (Renvela), and the iron-based sucroferric oxyhydroxide (Velphoro) and ferric citrate (Auryxia).
• To be most effective, give phosphate binders with each meal. Constipation is a frequent side effect; stool softeners may be needed.
• Aluminum preparations should be used with caution, because bone disease - osteomalacia - is associated with excess aluminum, and magnesium-containing antacids such as Maalox and Mylanta must not be used, because magnesium depends on the kidneys for excretion.

Hypocalcemia is a problem in the later stages of CKD due to the inability of the GI tract to absorb calcium in the absence of active vitamin D, and if it persists even when serum phosphate is normal, supplemental calcium and vitamin D may be given; if vitamin D levels are low it is given as cholecalciferol. But secondary hyperparathyroidism in ESRD requires the activated form of vitamin D because the kidneys cannot activate vitamin D - giving a precursor to an organ that cannot convert it does nothing. The chapter therefore names the already-active preparations, oral or IV calcitriol (Rocaltrol), IV paricalcitol (Zemplar), and oral or IV doxercalciferol (Hectorol), whose use can reduce high PTH levels by restoring calcium absorption and removing the stimulus.

• Cinacalcet (Sensipar), a calcimimetic agent, can control secondary hyperparathyroidism. Calcimimetics mimic calcium and increase the sensitivity of the calcium receptors in the parathyroid glands, so the glands detect calcium at lower serum levels and decrease PTH secretion. The drug does not raise calcium; it changes what the gland believes the calcium to be.
• If parathyroid disease becomes severe, a total parathyroidectomy is usually done and parathyroid tissue transplanted into the forearm. The transplanted cells make PTH as needed, and if PTH production becomes excessive some cells can be removed from the forearm - accessible without reopening the neck.
• Hypercalcemia may occur with calcium and vitamin D supplementation; if it does, vitamin D may be withheld and calcium-based phosphate binders replaced with non-calcium-based ones.

12.4 Anemia, Dyslipidemia, and Drug Dosing

For dyslipidemia, statins such as atorvastatin (Lipitor) can lower LDL cholesterol and should be used in patients with CKD, especially those with diabetes, not yet on dialysis, and fibrates such as gemfibrozil (Lopid) lower triglycerides and can increase HDLs. The governing principle for the rest of the medication list: the kidneys partially or totally excrete many drugs, so CKD causes decreased elimination that leads to accumulation and the potential for drug toxicity, and doses and frequency are adjusted based on the severity of the kidney disease. The drugs of particular concern are digoxin, diabetes agents (metformin, glyburide), antibiotics (vancomycin, gentamicin), and opioid drugs.

12.5 Nutrition Therapy - the Table and Its Disagreements

The chapter is frank that the diet itself is a hazard. Calorie-protein malnutrition is a potential, serious problem resulting from altered metabolism, anemia, dental problems, anorexia, and nausea, with depression and complex diets that restrict protein, phosphorus, potassium, and sodium as further contributors. Frequent monitoring of laboratory tests and anthropometric measurements are needed, and all patients with CKD should be referred to a dietitian.

12.6 The Restrictions in Practice

• Water and other fluids are not routinely restricted in patients with CKD stages 1 to 5 who are not receiving hemodialysis; diuretics reduce retention, and patients on HD have a more restricted fluid intake than patients on PD.
• Foods that are liquid at room temperature - gelatin, ice - are counted as fluid intake.Space the fluid allotment throughout the day so the patient does not become thirsty, and limit intake so that weight gains are no more than 1 to 3 kg between dialyses.
• Teach avoidance of processed meats, canned soups and stews, cold cuts, and many dressings. Salt substitutes should be avoided in potassium-restricted diets because they contain potassium chloride - one of the highest-yield teaching points in the chapter, because the substitution looks like compliance and is a potassium load. Patients using PD do not usually need potassium restrictions and may need oral potassium supplementation because of the loss of potassium with dialysis exchanges.
• By ESRD, phosphate is limited to around 1 g/day.Foods high in phosphate include meat and dairy products, and many foods high in phosphate are also high in protein - so when patients eat a diet containing protein, phosphate binders are given to control the phosphate level.

12.7 Nursing Assessment and Health Promotion

• Obtain a complete history of existing or family kidney disease. Alport syndrome and polycystic kidney disease have a genetic component; other problems leading to CKD are diabetes, hypertension, and systemic lupus erythematosus.
• Obtain a medication history, because many drugs are nephrotoxic. Decongestants and antihistamines containing pseudoephedrine and phenylephrine cause vasoconstriction and increase BP; magnesium and aluminum from antacids accumulate because they cannot be excreted; and NSAIDs can contribute to AKI and progression of CKD, especially in higher than recommended doses, though taken as prescribed these analgesics are usually considered safe.
• Assess diet habits, measure height and weight, and evaluate recent weight changes.Assess support systems - the choice of treatment may be related to the support available. The four clinical problems are fluid imbalance, electrolyte imbalance, impaired cardiac function, and difficulty coping, and expected outcomes are fluid and electrolyte levels within normal ranges and an acceptable weight with no more than a 10% weight loss.
• Identify those at risk - people with diabetes or hypertension or a personal or family history of kidney disease or repeated UTIs - for regular checkups including routine urinalysis and calculation of the estimated GFR. People with diabetes need their urine checked for albuminuria if routine urinalysis is negative for protein.
• Most important are measures to reduce the risk or progression of cardiovascular disease - glycemic control, BP control, and lifestyle modifications including smoking cessation. The chapter's population health box: early detection and treatment are the ways to reduce CKD; ensure diagnosis and treatment of diabetes as the leading cause; monitor BP to detect elevations early; and treat hypertension appropriately as the second leading cause.

12.8 Patient and Caregiver Teaching, and Ambulatory Care

• Most of the care of the patient with CKD occurs on an outpatient basis. In-hospital care is needed for management of complications and kidney transplant.
• Because patients take many medications, a pillbox organizer or a list of the drugs and times of administration may be helpful, and the patient should avoid OTC drugs such as NSAIDs and aluminum- and magnesium-based laxatives and antacids. Teach daily BP readings and watching for fluid overload, hyperkalemia, and other electrolyte imbalances.
• The patient can complete a transplant evaluation before dialysis is needed and may receive a transplant before ever starting dialysis, though the shortage of donor organs limits this for many. Most patients need either PD or HD, and most use HD.Tell the patient that even while on dialysis transplant is still an option, and that if a transplanted organ fails the patient can return to dialysis.
• Discuss palliative care as needed - patients often start the conversation. Focus on moving from a curative approach to promotion of comfort care and consideration of hospice, allow them to do most of the talking, and pay special attention to their hopes and fears.

12.9 The Older Adult With CKD, and Withdrawal From Treatment

• The incidence of CKD is increasing most rapidly in older adults, and the most common diseases leading to CKD in older adults are hypertension and diabetes. Care is complicated by decreased cardiopulmonary function, bone loss, immunodeficiency, altered protein synthesis, impaired cognition, and altered drug metabolism.
• Malnutrition is common, from lack of mobility, social isolation, physical disability, and impaired cognitive function - four causes a diet sheet will not fix.
• Modality choice rests on physical and emotional health, personal preferences, and availability of support. Quality-of-life measures show no justification for excluding the older adult from dialysis programs, and rationing dialysis based on age alone is not a reasonable decision for health care professionals to make.
• Older adults have used dialysis successfully, especially peritoneal dialysis, though many choose in-center hemodialysis for lack of help at home, and establishing vascular access for HD may be difficult because of atherosclerotic changes. Transplant is possible, but older adults are carefully screened to ensure the benefits outweigh the risks.

13.1 What Dialysis Is, and When It Starts

Dialysis is the movement of fluid and molecules across a semipermeable membrane from one compartment to another. Clinically, substances move from the blood through a semipermeable membrane and into a dialysis solution called dialysate. It corrects fluid and electrolyte imbalances and removes waste products in kidney failure, and can also be used to treat drug overdoses. In PD the peritoneal membrane is the semipermeable membrane; in HD an artificial cellulose-based or synthetic membrane is used.

• Dialysis is started when uremia can no longer be adequately treated with conservative medical management - generally when the GFR is less than 15 mL/min/1.73 m2.The nephrologist decides based on the patient's clinical status.
• Certain uremic complications indicate a need for immediate dialysis: encephalopathy, neuropathies, hyperkalemia, pericarditis, and accelerated hypertension.
• Most ESRD patients are dialyzed rather than transplanted because of a lack of donated organs, unsuitability for transplant, or patient preference. A patient's age is not a factor in determining candidacy for dialysis.

13.2 The Three Physical Principles

13.3 Peritoneal Dialysis - the Catheter, the Exchange, and the Systems

• Access is a catheter through the anterior abdominal wall, about 24 in (60 cm) long, with 1 or 2 Dacron cuffs that act as anchors and prevent the migration of microorganisms into the peritoneum; fibrous tissue grows into the cuff within a few weeks. It is usually placed surgically so the catheter can be seen directly.PD may be started at once with low-volume exchanges or delayed for 2 weeks pending healing and sealing of the exit site.
• In PD it is critical to maintain aseptic technique to avoid peritonitis, and all patients are taught to check the site for infection. Once healed the patient may shower and pat the site dry; showering is preferred to bathing.
• Exchange volume is mainly determined by the size of the peritoneal cavity - 2 L for an average-size person, 3 L for a larger one, smaller volumes for a smaller body, pulmonary compromise, or inguinal hernias.
• Dextrose is the most often used osmotic agent, safe and inexpensive but associated with high rates of peritoneal glucose absorption, leading to hypertriglyceridemia, hyperglycemia, and long-term peritoneal membrane dysfunction. Icodextrin is iso-osmolar and induces ultrafiltration by its oncotic effect; amino acid solutions serve patients needing nutrition supplementation.

The 3 phases of the PD cycle are inflow (fill), dwell (equilibration), and drain. Together, the 3 phases are an exchange, and a manual exchange takes about 30 to 50 minutes.

• Automated peritoneal dialysis (APD) is the most popular form of PD because it allows patients to do dialysis while they sleep. A cycler times the phases and runs 4 or more exchanges per night with 1 to 2 hours per exchange; the patient disconnects in the morning and usually leaves fluid in the abdomen during the day. It is hard to achieve the required clearance solely with nighttime APD; 1 or 2 daytime manual exchanges may be needed.
• Continuous ambulatory peritoneal dialysis (CAPD) is done every few hours during the day - 2 L 4 times daily, dwell times averaging 4 hours, on a schedule such as 7 am, 12 noon, 5 pm, and 10 pm. The patient instills 2 to 3 L, disconnects the bag and line, then reconnects after equilibration to drain and refill.

13.4 Peritoneal Dialysis - Complications and Effectiveness

13.5 Hemodialysis - Access, Dialyzer, and Schedule

HD requires a very rapid blood flow and access to a large blood vessel. Obtaining vascular access is one of the biggest problems associated with HD.

The HD dialyzer is a plastic cartridge that has thousands of parallel hollow tubes or fibers of semipermeable membrane. Blood is pumped into the top and dispersed into all the fibers; dialysate is pumped into the bottom and bathes the outside of the fibers, where ultrafiltration, diffusion, and osmosis occur across the pores before the blood converges into a single tube that returns it to the patient. Dialyzers differ in surface area, membrane composition and thickness, clearance of waste products, and removal of fluid.

• The needles are large bore, usually 14 to 16 gauge.The needle closer to the fistula, the red catheter lumen, pulls blood to the dialyzer using a blood pump; blood returns through the second needle, the blue lumen.Heparin is added, because blood in contact with a foreign material tends to clot, and the dialysate runs countercurrent to the blood flow. To end the treatment, saline returns the blood in the circuit to the patient, then firm pressure is applied until bleeding stops.
• Before treatment, assess fluid status - weight, BP, peripheral edema, lung and heart sounds - the vascular access, and temperature.The difference between the last postdialysis weight and the present predialysis weight determines the ultrafiltration.During HD, take vital signs at least every 30 to 60 minutes, because rapid BP changes may occur.
• Most HD patients dialyze in a community-based center for 3 to 4 hours, 3 days per week.Long nighttime HD is 6 to 8 hours up to 6 times per week; short daily HD is 2.5 to 3 hours, 5 to 6 days per week, usually at home.Daily or nighttime dialysis brings fewer uremic symptoms, fewer medications, and fewer side effects such as hypotension and cramps - yet only about 2% of HD patients dialyze at home.

13.6 Hemodialysis - Complications, and the Comparison With PD