MEDICINE 2

Professor: DR. OLIVER LACAMBRA Trans by: Agcaoili, Echavari, Llena,

Wacas, Zamora
TOPIC: NEUROLOGIC CRITICAL CARE (4-16-23)

LOCKED-IN STATE
OUTLINE
• pseudocoma
I. Coma
II. Brain Death • awake but no means to produce speech or volitional
III. Severe Acute Encephalopathies and Critical Care limb movements
Weakness • retains voluntary vertical eye movements & lid
IV. Critical Care Disorders of the Central Nervous System elevation
V. Critical Care Disorders of the Peripheral Nervous System
• infarction or hemorrhage at the ventral pons

I. COMA ANATOMY & PHYSIOLOGY OF COMA

1. widespread abnormalities of the cerebral hemisphere
• most severe form of state of reduced alertness 2. reduced activity of a thalamocortical alerting system
• deep sleeplike state, eyes closed, unarousable (RAS)
• stupor
o higher degree of arousability, can be awakened COMA DUE TO CEREBRAL MASS LESIONS &
by vigorous stimuli HERNIATION SYNDROMES
● HERNIATION
• drowsiness
○ displacement of brain tissue by an overlying or
o simulates light sleep, easy arousal & the
adjacent mass into a contiguous compartment
persistence of alertness for brief periods
● produce “false localizing” signs
• stupor & drowsiness are usually accompanied by some
● transtentorial herniation - most common
degree of confusion
• lethargy, semicoma, obtundation
COMA DUE TO METABOLIC DISORDERS & TOXINS
1. interrupt delivery of energy substrate
VEGETATIVE STATE
2. alter neuronal excitability
• awake-appearing but non responsive state
• the eyelids may open periodically CBF in:
• respiratory & autonomic functions are retained - ● gray matter = 75ml/100g/min
yawning, coughing, swallowing, limb & head ● white matter = 30ml/100g/min
movements persist Oxygen consumption = 3.5ml/100g/min
• decerebrate or decorticate limb posturing, absent Glucose utilization = 5mg/100g/min
responses to visual stimuli
• cardiac arrest with cerebral hypo perfusion & head APPROACH TO THE PATIENT
trauma are the most common causes ● acute respiratory & cardiovascular problems prior to
neurologic assessment
AKINETIC MUTISM ● useful points:
• partially or fully awake state in which the patient is able a) neurologic symptoms
to form impression & think; virtually immobile & mute b) antecedent symptoms
o medial thalamic nuclei c) use of medications, drugs, alcohol
o frontal lobes d) chronic diseases
o extreme hydrocephalus
GENERAL PHYSICAL EXAMINATION
ABULIA ● fever
• milder form ● tachypnea
• mental & physical slowness & diminished ability to ● hypotension, hypertension
initiate activity ● fundoscopic exam (papilledema)
• damage to medial frontal lobes ● petechiae
● cyanosis, pallor
CATATONIA
• hypomobile & mute syndrome NEUROLOGIC EXAMINATION
• occurs usually as part of major psychosis ● 1st observe without intervention
• few voluntary or responsive movements ● drowsy signs
• they blink, swallow, not appear distressed ● hemiplegia
• “waxy flexibility” or catalepsy ● hemiparesis
● seizures
● asterixis sign

Page 1 of 8
 ● decerebrate ● corneal reflex - cranial nerves 5 & 7, pontine function
○ damage to motor tracts caudal to the
midbrain C. RESPIRATORY PATTERNS
● decorticate ● shallow, slow, regular - metabolic or drug
○ bilateral damage rostral to the midbrain ● Cheyne-stokes - bihemispheral damage or metabolic
suppression
LEVEL OF AROUSAL ● Rapid deep breathing (kussmaul) - metabolic
● sequence of increasingly intense stimuli acidosis, pontomesencephalic lesion
● tickling of nostrils with a cotton wisp ● Agonal gasps - lower brainstem damage
● pressure on the knuckles or bony prominence - terminal respiratory pattern
● pinprick, skin pinching
● posturing in response to noxious stimuli → severe LABORATORY STUDIES AND IMAGING
damage to corticospinal system
● unilateral posturing • chemical-toxicologic analysis
• cranial CT or MRI
BRAINSTEM REFLEXES • EEG
• cranial nerves nuclei & RAS are located in the • CSF examination
brainstem • ABGs
o pupillary size & reaction to light • Blood chemistry
o spontaneous & elicited eye movements
o corneal responses DIFFERENTIAL DX OF COMA
o respiratory pattern
• causes of sudden coma:
A. PUPILLARY SIGNS a) drug ingestion
● in bright diffuse light b) cerebral hemorrhage
● reactive & round pupils (2.5-5mm) c) Trauma
● 1 enlarged & poorly reactive d) Cardiac arrest
○ compression or stretching of the 3rd nerve e) epilepsy
● oval, sl. eccentric pupil -early midbrain and 3rd nerve • subacute coma: pre-existing medical condition,
compression neuro problem, secondary brain swelling
● dilated bilateral, non-reactive - severe midbrain
damage
● small reactive bilateral but not pinpoint
a) metabolic encephalopathies
b) hydrocephalus
c) thalamic hemorrhage
● smaller reactive pupils (<1mm)
a) narcotic or barbiturate overdose
b) extensive pontine hemorrhage

B. OCULAR MOVEMENTS
● elevate the lid & observe resting position &
spontaneous movements of the globes
● horizontal divergence - drowsiness - conjugate
horizontal roving - spontaneous eye movements in
coma
● conjugate horizontal ocular deviation one side
○ damage to frontal lobe on the same side; pons
on the opposite side
○ “ the eyes look toward a hemispherical lesion
and away from a brainstem lesion”
● frontal lobe seizures - drive the eyes to the opposite
side
● thalamic & upper midbrain lesion - eye turn down &
inward
● bilateral pontine damage - “ocular bobbing”
● diffuse cortical anoxic damage - “ocular dipping”
● “doll’s eye”
● oculovestibular response - nystagmus in the
opposite direction

Page 2 of 8
 • CVD cause of coma: PATHOPHYSIOLOGY
1) basal ganglia and thalamic hemorrhage
2) pontine hemorrhage Brain Edema
3) cerebellar hemorrhage
4) basilar artery thrombosis - 2 principal types of edema are:
5) subarachnoid hemorrhage 1. vasogenic - influx of fluid and solutes into the brain
through an incompetent blood-brain barrier (BBB)
II. BRAIN DEATH
2. cytotoxic - cellular swelling, membrane breakdown,
and ultimately cell death
• state of irreversible cessation of all cerebral and
brainstem function with preservation of cardiac activity Ischemic Cascade and Cellular Injury
and maintenance of respiratory and somatic function
by artificial means ● Penumbra - areas of ischemic brain tissue that have
• recognized as morally, ethically, and legally equivalent not yet undergone irreversible
to death ● systemic hypotension and hypoxia exacerbate
ischemic injury
CRITERIA ● fever, seizures, and hyperglycemia increase cellular
metabolism
1) widespread cortical destruction that is reflected by ● Prevention, identification, and treatment of secondary
deep coma and unresponsive- ness to all forms of brain insults are fundamental goals of management
stimulation ● Apoptosis (programmed cell death)

2) global brainstem damage demonstrated by absent Cerebral Perfusion and Autoregulation

pupillary light reaction, absent corneal reflexes, loss of
oculovestibular reflexes, and destruction of the ● CPP= MAP - ICP
medulla, manifested by complete and irreversible ● Autoregualtion refers to the physiologic response
apnea whereby CBF is regulated via alterations in
cerebrovascular resistance
• apnea is due to medullary damage requires that the ● CBF is influenced by pH and PaCO2
Pco2 be high enough to stimulate respiration during a ● CBF is increased with hypercapnia and acidosis and
test of spontaneous breathing decreased with hypocapnia and alkalosis
• isoelectric EEG
Cerebrospinal Fluid (CSF) and ICP
TREATMENT
● brain, CSF, and blood
• prevention of further nervous system damage ● ~ 150 mL of CSF
(immediate goal in comatose patient) ● cerebral blood volume is also ~150 mL
• hypotension, hypoglycemia, hypercalcemia, hypoxia, ● obstruction of CSF outflow, edema of cerebral
hypercapnia, and hyperthermia should be corrected ● tissue, or increases in volume from tumor or hematoma
rapidly may increase ICP
• Tracheal intubation is indicated if there is apnea, ● ↑ICP → ↓cerebral perfusion → ischemia →
hypoventilation, or emesis, or if the patient is at risk for vasodilation → ↑cerebral blood volume → ↑ICP
aspiration
• IV access APPROACH TO THE PATIENT
• hypnotic IV solution
SEVERE BRAIN DYSFUNCTION
PROGNOSIS
• determine the cause (diffuse or focal)
• metabolic comas have better prognosis • minor focal deficits may be present in patients with
• GCS coma scale metabolic encephalopathies
• poor outcome, persistent vegetative state • prominent focal signs should suggest the possibility of
a structural lesion
III. SEVERE ACUTE ENCEPHALOPATHIES AND CRITICAL • all patients with a decreased level of consciousness
CARE WEAKNESS associated with focal findings should undergo an
urgent neuroimaging procedure, as should all patients
Neurologic critical care focuses on: with coma of unknown etiology.
• acute brainstem ischemia due to basilar artery
a) preservation of neurologic tissue
thrombosis may cause generalized seizures
b) prevention of secondary brain injury
• CT scan may reveal a hyperdense basilar artery
- Encephalopathy is a general term describing brain
indicating thrombus in the vessel
dysfunction that is diffuse, global or multi-focal
• subsequent CT or MR angiography can assess basilar
artery patency

Page 3 of 8
 • EEG of metabolic encephalopathy typically reveals
generalized slowing.
• CT scan for initial study
• MRI more specific information in acute ischemic stroke
• neurovascular imaging using CT or MRI angiography
or venography
• EEG of metabolic encephalopathy typically reveals
generalized slowing
• EEG to help exclude inapparent seizures, especially
nonconvulsive status epilepticus.

PATHOPHYSIOLOGY

• lumbar puncture may be necessary to exclude

infectious or inflammatory processes
• serum electrolytes (especially sodium and calcium),
glucose, renal and hepatic function, CBC, and
coagulation
• serum or urine toxicology screens should be performed
in patients with encephalopathy of unknown cause
• monitoring of ICP: primary neurologic disorders, stroke
or traumatic brain injury others:
a) severe traumatic brain injury (GCS<8)
b) large tissue shifts from supratentorial ischemic or
hemorrhagic stroke TREATMENT OF ELEVATED ICP
c) hydrocephalus from SAH
● ICP should be maintained at <20 mmHg and CPP
d) intraventricular hemorrhage
should be maintained at ≥60 mmHg
e) posterior fossa stroke
● in trauma/stroke: mannitol or hypertonic saline
f) fulminant hepatic failure
● early signs of elevated ICP include drowsiness and a
• ventriculostomy is preferable to ICP monitoring devices
diminished level of consciousness
in the brain parenchyma
● hypotonic IV fluids should be avoided
• ICP monitoring is most appropriate for patients with
● elevation of the head of the bed
diffuse edema and small ventricles
● emergent treatment of elevated ICP is most quickly
achieved by intubation hyperventilation
● high-dose barbiturates, decompressive
hemicraniectomy, and hypothermia are used for
refractory elevations of ICP
● decompressive hemicraniectomy has been shown to
improve outcome in select patients.

SECONDARY BRAIN INSULTS

• prevent secondary brain injury

• avoid hypotension (<90mmHg systolic)
• avoid hypoxia ( < 90% O2 sat)
• control fever & hyperglycemia

IV. CRITICAL CARE DISORDERS OF THE CENTRAL

NERVOUS SYSTEM

HYPOXIC ISCHEMIC ENCEPHALOPATHY

A. CLINICAL MANIFESTATIONS
● MILD: impaired judgment, inattentiveness, motor
incoordination, and, at times, euphoria
● circulatory arrest: LOC in seconds
○ restored within 3–5 min, full recovery
○ beyond 3–5 min, some degree of permanent
cerebral damage

Page 4 of 8
 • Brain is more tolerant to pure hypoxia than it is to ● older patients are particularly vulnerable to delirium, a
hypoxia-ischemia confusional state: disordered perception, frequent
hallucinations, delusions, and sleep disturbance
B. CLINICAL MANIFESTATIONS ● cause of delirium is often multifactorial
● hypercarbic encephalopathy can present with
• prognosis is better for patients with intact brainstem headache, confusion, stupor, or coma
function: ● hypoventilation syndrome - ↑Paco2 leading to CO2
a) normal pupillary light responses narcosis may have a direct anesthetic effect, and
b) intact oculocephalic (doll’s eyes) reflex cerebral vasodilation from ↑Paco2 → ↑ ICP
c) intact oculovestibular (caloric) reflex ● hyperglycemia and hypoglycemia
d) intact corneal reflexes ● hypernatremia and hyponatremia

C. PATHOLOGY SEPSIS-ASSOCIATED ENCEPHALOPATHY

● extensive multifocal or diffuse laminar cortical necrosis
with frequent involvement of the hippocampus A. PATHOGENESIS
● scattered small areas of infarction or neuronal loss may ● inflammatory mediators → encephalopathy
be present in the basal ganglia, hypothalamus, or ● sepsis-associated encephalopathy :patients with
brainstem critical illness, sepsis, or SIRS develop
● watershed infarcts cause cognitive deficits, including encephalopathy without obvious explanation
visual agnosia, and weakness that is greater in ● systemic inflammatory response syndrome (SIRS),
proximal than in distal muscle groups. can lead to multisystem organ failure
● interleukin (IL)-1, IL-2, and IL-6 are thought to play a
D. DIAGNOSIS role in this syndrome.
● history of a hypoxic-ischemic event such as cardiac
arrest B. DIAGNOSIS
● <70 mmHg systolic BP or Pao2 <40 mmHg is usually ● a diffuse dysfunction of the brain without prominent
necessary focal findings
● both absolute levels and duration of exposure are ● confusion, disorientation, agitation, and fluctuations in
important determinants of cellular injury level of alertness
● carbon monoxide intoxication ● hyperreflexia and frontal release signs such as a grasp
or snout reflex
E. TREATMENT ● myoclonus, tremor, or asterixis
● directed at restoration of normal cardiorespiratory
function OSMOTIC DEMYELINATION SYNDROME (CENTRAL
● securing a clear airway, ensuring adequate PONTINE MYELINOLYSIS)
oxygenation and ventilation, and restoring cerebral
● quadriplegia and pseudobulbar palsy
perfusion, whether by cardiopulmonary resuscitation,
● predisposing factors:
fluid, pressors, or cardiac pacing
a) severe underlying medical illness
● hypothermia (33C) may target the neuronal cell injury
b) nutritional deficiency
cascade
c) rapid correction of ↓ Na (most cases)
● TTM = 32-36C for 24 hours
● demyelination without inflammation in the base of the
○ risk: coagulopathy & infection
pons, with relative sparing of axons and nerve cells
● carbon monoxide intoxication may be treated with
hyperbaric oxygen
● anticonvulsants for seizures

POST CARDIAC BYPASS BRAIN INJURY

● are common and include:

a) acute encephalopathy
b) stroke
c) chronic syndrome of cognitive impairment
● hypoperfusion and embolic disease are frequently
involved in the pathogenesis
● embolic disease is likely the predominant mechanism
of cerebral injury during cardiac symptoms

METABOLIC ENCEPHALOPATHIES

● altered mental states: confusion, delirium,

disorientation, and encephalopathy

Page 5 of 8
 WERNICKE’S DISEASE

• preventable disorder due to a deficiency of thiamine

• alcoholics account for most cases
• patients with malnutrition due to hyperemesis,
• starvation, renal dialysis, cancer, HIV/AIDS - triad of
ophthalmoplegia, ataxia, and global confusion
• disoriented, indifferent, and inattentive - stupor, coma,
death may ensue
• findings:
1. horizontal nystagmus on lateral gaze
2. lateral rectus palsy (usually bilateral)
3. conjugate gaze palsies, and rarely ptosis
4. gait ataxia
• pupils spared; biotic in advanced disease
• usually associated with polyneuropathy V. CRITICAL CARE DISORDERS OF THE PERIPHERAL
• Korsakoff’s psychosis - amnestic state with NERVOUS SYSTEM (PNS)
impairment in recent memory and learning
• critical illness with disorders of the PNS arises in two
contexts:
A. PATHOLOGY
1. primary neurologic diseases that require critical
care intervention
• periventricular lesions surround the third ventricle,
a. acute polyneuropathies such as GBS,
aqueduct, and fourth ventricle
neuromuscular junction disorders myasthenia
• petechial hemorrhages in occ’l acute cases
gravis and botulism
• atrophy of the mammillary bodies in most chronic
2. secondary PNS manifestations of systemic critical
cases
illness
• endothelial proliferation, demyelination, and some a. from systemic disease
neuronal loss
• amnestic defect is related to lesions in the dorsal
• assessment of pulmonary mechanics:
medial nuclei of the thalamus a) maximal inspiratory force (MIF)
b) vital capacity (VC)
B. PATHOGENESIS c) evaluation of strength of bulbar muscles
• thiamine deficiency produces a diffuse decrease in • endotracheal intubation should be considered when the
cerebral glucose utilization and results in mitochondrial MIF falls to below –25 cmH2O or the VC is <1 L
damage
• severe palatal weakness may require endotracheal
• glutamate accumulates → excitotoxic cell damage
intubation

NEUROPATHY

• PNS dysfunction is present in patients with prolonged

critical illnesses
• failure to wean from mechanical ventilation
• critical illness polyneuropathy - most common PNS
complication r/t critical illness
• neurologic findings: diffuse weakness, ↓reflexes, and
distal sensory loss
• circulating factors such as cytokines, which are
C. TREATMENT
associated with sepsis and SIRS
• up to 70% of patients with the sepsis syndrome have
• medical emergency
some degree of neuropathy
• administration of thiamine, 100 mg IV/IM
• aggressive glycemic control with insulin infusions
• dose should be given daily until the patient resumes a
appears to decrease the risk of critical illness
normal diet
polyneuropathy
• should be given prior to glucose IV solution
• supportive treatment
• thiamine should be administered to all alcoholic
patients requiring parenteral glucose.
DISORDERS OF NEUROMUSCULAR TRANSMISSIONS

• botulinum toxin from improperly stored food

Page 6 of 8
• diplopia and dysphagia are early signs of food- borne ● 85% occur in the anterior circulation, mostly on the
botulism circle of Willis
• weakness from impaired neuromuscular junction ● the arterial internal elastic lamina disappears at the
transmission (drugs: aminoglycosides, beta-blockers, base of the neck
muscle relaxants) ● the media thins, and connective tissue replaces
• once the offending medications are discontinued, full smooth-muscle cells
strength is restored ● Dome - most often site of rupture
● Aneurysm size and site are important in predicting risk
MYOPATHY of rupture
● Greater risk of rupture:
• muscle weakness and wasting, often in the face of a) >7 mm in diameter
b) Those at the top of the basilar artery
seemingly adequate nutritional support
c) and at the origin of the posterior communicating
• critical illness myopathy - catabolic myopathy may artery
develop as a result of multiple factors, including
elevated cortisol and catecholamine release and other
circulating factors induced by the SIRS SACCULAR (“BERRY”) ANEURYSM CLINICAL
• cachectic myopathy - serum creatine kinase levels MANIFESTATIONS
and electromyography (EMG) are normal
• muscle biopsy shows type II fiber atrophy • unruptured intracranial aneurysms are completely
• panfascicular muscle fiber necrosis asymptomatic
• acute necrotizing intensive care myopathy is • increase ICP
characterized clinically by weakness progressing to a • sudden transient loss of consciousness occurs in
profound level nearly half of patients
• pathologically, there may be loss of thick (myosin) • excruciating headache
filaments • presenting symptom in about 45% of cases
• “the worst headache of my life”
SUBARACHNOID HEMORRHAGE • vomitting & neck stiffness
• sudden headache in the absence of focal neurologic
• renders the brain critically ill from both primary and symptoms is the hallmark of aneurysmal rupture
secondary brain insults • third cranial nerve palsy occurs at the junction of the
• trauma, aneurysm, AV malformations posterior communicating artery and the internal carotid
• some idiopathic SAHs are localized to the artery
perimesencephalic cisterns and are benign • sixth nerve palsy may indicate an aneurysm in the
cavernous sinus
SACCULAR (“BERRY”) ANEURYSM • occipital and posterior cervical pain may signal a
posterior inferior cerebellar artery or anterior inferior
● mortality rate over the next month is about 45% cerebellar artery aneurysm
● of those who survive, more than half are left with major • pain in or behind the eye and in the low temple can
neurologic deficits: initial hemorrhage, cerebral occur with an expanding MCA aneurysm
vasospasm with infarction, or hydrocephalus • sentinel bleeds = leak of blood into the subarachnoid
● rate of rebleeding is about 20% in the first 2 weeks, space
30% in the first month, and about 3% per year • sudden unexplained headache at any location should
afterward raise suspicion of SAH
• the annual risk of rupture for aneurysms <10 mm in • the initial clinical manifestations of SAH can be graded
size is ~0.1%, and for aneurysms ≥10 mm in size is using the Hunt-Hess or World Federation of
~0.5–1% Neurosurgical Societies classification schemes

● giant aneurysms, (>2.5 cm) occur at the same account

for 5% of cases
● three most common locations:
1. terminal internal carotid artery
2. middle cerebral artery (MCA) bifurcation
3. top of the basilar artery
● mycotic aneurysms are usually located distal to the first
bifurcation of major arteries of the circle of Willis
● infected emboli due to bacterial endocarditis
● bifurcations of the large- to medium-sized intracranial
arteries
● rupture is into the subarachnoid space in the basal
cisterns and of the adjacent brain

Page 7 of 8
 DELAYED NEUROLOGIC DEFICITS • 2D-echo: pattern of regional wall motion abnormalities

4 major causes of delayed neurologic deficits:

1. rerupture
2. hydrocephalus
3. delayed cerebral ischemia (DCI)
4. hyponatremia.

A. RERUPTURE
• 30% incidence in the 1st month following SAH -
associated with a 50% mortality rate and poor outcome
- early treatment

B. HYDROCEPHALUS

• cause stupor and coma TREATMENT

• placement of external centrically drain - CT scan
• may clear spontaneously • early aneurysm repair prevents rerupture
• chronic - weeks to months • improve blood flow in vasospasm & ischemia
• gait difficulty, incontinence, or impaired mentation • aneurysmal clipping or coiling
• metal clip across the aneurysm neck
C. DELAYED CEREBRAL ISCHEMIA • endovascular techniques involve placing platinum
coils, or other embolic material
• vasospasm - cause symptomatic ischemia and o < risk of death; > rebleeding
infarction in ~30% of patients • newer endovascular techniques:
o major cause of delayed morbidity and death a) balloon-assisted coiling
o result from direct effects of clotted blood and its b) placement of flow-diverting stents
breakdown products
o x-ray angiography MEDICAL
o may increase ICP 1. protect the airway
• signs of DCI appear 4–14 days after the hemorrhage 2. manage blood pressure before and after aneurysm
treatment
3. prevent rebleeding prior to treatment 4. manage
D. HYPONATREMIA vasospasm and DCI
4. treat hydrocephalus
• may be profound and can develop quickly in the first 2 5. treat hyponatremia
weeks following SAH 6. limit secondary brain insults
7. prevent pulmonary embolus (PE)
• natriuresis and volume depletion
• stuporous patient should undergo emergent
• “cerebral saltwasting syndrome”
ventriculostomy to measure ICP and to treat high ICP in
• clears over the course of 1–2 weeks
order to prevent cerebral ischemia
• should not be treated with free-water restriction as this
• maintain adequate cerebral perfusion pressure
may increase the risk of stroke
• avoiding excessive elevation of arterial pressure
• lower the systolic blood pressure <160mmHg - cerebral
LABORATORY EVALUATION & IMAGING
perfusion pressure targeted to 60–70 mmHg
• headache or neck pain is severe, mild sedation and
• hallmark: blood in the cerebrospinal fluid (CSF)
analgesia - adequate hydration
• > 95% seen on CT scan
• steroid may help reduce the head and neck pain
• lumbar puncture (xantochromic CSF)
• DCI: calcium channel antagonist Nimodipine (60 mg PO
• extent and location of blood on a CTscan:
every 4 h)
1. locate the underlying aneurysm
2. identify the cause of any neurologic deficit • consider induced hypertension and hypervolemia
3. predict the occurrence of vasospasm • chronic hydrocephalus develops, ventricular shunting is the
treatment of choice
• four-vessel conventional x-ray angiography (both • free-water restriction is contraindicated in patients with SAH
carotids and both vertebrals) at risk for DCI
• CT angiography is an alternative method for locating • all patients should have pneumatic compression stockings
the aneurysm and may be sufficient to plan definitive Reference:
therapy • Dr. Lacambra ppt
• Loscalzo, J., Kasper, D. L., Longo, D. L., Fauci, A. S.,
• close monitoring of electrolytes Hauser, S. L., & Jameson, J. L. (2022). Harrison's Principles
• ECG - same with cardiac schema of Internal Medicine (21st ed., Vol. I). McGraw Hill.
• asymptomatic troponin elevation is common

Page 8 of 8