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TABLE36.2 CLASSIFICATION AND TREATMENT OFHEPATIC ENCEPHALOPATHY
Grade I
Grade II gross disorientation, drowsiness, +/
transfer to liver transplantation facility transfer to liver transplantation facility
consider listing for liver transplantation consider listing for liver transplantation
obtain head CT to rule out other causes of altered mental status intubate and hyper ventilate
avoid sedation and stimulation elevate head of bed
administer lactulose consider intracranial pressure monitor
CASE- BASED LEARNING DISCUSSION
Behavioral changes with minimal changes in
consciousness
- asterixis, inappropriate behavior
Grade III
Grade IV comatose, unresponsive to pain,
treat seizures
administer mannitol and hypertonic saline
hepatic function. Measurement of intraoperative
Marked confusion, incoherent speech, drowsy
but arousable to vocal stimuli
decorticate/ decerebrate posturing
ammonia levels may be indicated in patients with
1. Are halogenated, volatile anesthetics hepatotoxic?
e question has been posed for decades, beginning
with the identication of “halothane hepatitis” as a
clinical entity in the 1960s. e precise mechanism
for “halothane hepatitis’ has never been clearly
established. Although the incidence of serious hepatic
dysfunction aer exposure to sevourane or desurane
is extremely low, there are sporadic case reports in
the medical literature. Since there are other reasons
to avoid halogenated anesthetics in this patient
(encephalopathy), TIVA would be a better choice.
2. How does acetaminophen cause acute liver failure?
Large doses of acetaminophen overwhelm the
liver’s capacity for sulfation and glucuronidation.
As a consequence NAQPI, a toxic intermediate,
causes centrilobular necrosis. Administration of
N-acetylcysteine within 10 hours of acetaminophen
overdose helps reduce NAQPI. e toxic dose of
acetaminophen is 200mg/ kg.
3. Should any patient with moderate to severe
hepatic dysfunction be considered to be at risk for
encephalopathy? Encephalopathy is a signicant
cause of mortality in patients with liver failure.
e cerebral edema is caused by hyperammonemia,
neuroinammation, alterations in neurotransmission,
and a disturbance in cerebral autoregulation. It is
possible that perioperative physiologic derangements
that reduce hepatic blood ow could precipitate acute
liver failure in a patient with marginal preexisting
moderate to severe hepatic dysfunction. Increasing
ammonia levels or an ammonia level greater than 143
micromol/ L should prompt treatment for impending
cerebraledema.
4. Are patients with moderate hepatic dysfunction at risk
for nonhepatic perioperative complications? Patients
with preexisting liver disease such as cirrhosis frequently
have other comorbidities such as diabetes, hypertension,
and pulmonary disease. ese patients experience a
higher risk of postoperative infection, pneumonia,
acute renal failure, and coagulopathy. Whether the
type of anesthesia inuences outcome inpatients with
moderate hepatic dysfunction is notclear.
5. Why are patients with cirrhosis at risk for acute
renal failure? Patients with cirrhosis have portal
hypertension that through a variety of mechanisms
results in pooling of blood in the splanchnic system
and a subsequent decrease in the circulating blood
volume. Sympathetic activation causes a compensatory
increase in cardiac output in order to maintain renal
perfusion. Superimposed sepsis or hypovolemia from
any cause may compromise compensatory mechanisms
and reduce renal perfusion, resulting in acute kidney
injury (AKI), dened as an increase in the serum
creatinine of > 50% of baseline or an absolute rise in
creatinine of > 0.3 mg/ dL in less than 48 hours. e
pathophysiology of renal dysfunction in patients with
cirrhosis is complex, but volume expansion should be
the immediate therapeutic response.
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REFERENCES
6. Bunchorntavakul C, Reddy KR. Acetaminophen- related hepatotoxicity. Clinical Liver Disease. 2013;17:587– 607.
1. Bernal W, Wendon J. Acute liver failure. New England Journal of
Medicine. 2013;369:2525– 34.
2. Shalimar SKA. Management in acute liver failure. Journal of Clinical
and Experimental Hepatology. 2015;5:S104– 15.
3. Jayakumar AR, Rao KVR, Norenberg MD. Neuroinammation in
hepatic encephalopathy: mechanistic aspects. Journal of Clinical
and Experimental Hepatology. 2015;5:S21– 8.
4. Munoz SJ, Stravitz RT, Gabriel DA. Coagulopathy of acute liver
failure. Clinical Liver Disease. 2009;13:95– 107.
5. Krisl JC, Meadows HE, Greenberg CS, Mazur JE. Clinical useful-
7. Hodgman MJ, Garrard AR. A review of acetaminophen poisoning.
Critical Care Clinics. 2012;28:499– 516.
8. Glassford NJ, Farley KJ, Warrillow S, Bellomo R. Liver transplantation rapidly stops cerebral ammonia uptake in fulminant hepatic
failure. Critical Care and Resuscitation Journal. 2011;13:113– 18.
9. O’Grady J. Timing and benet of liver transplantation in acute liver
failure. Journal of Hepatology. 2014;60:663– 70.
10. Dear JW, Antoine DJ. Stratication of paracetamol overdose
patients using new biomarkers:current candidates and further challenges. Expert Review of Clinical Pharmacology. 2014;7:181– 9.
ness of recombinant activated factor VII in patients with liver failure undergoing invasive procedures. Annals of Pharmacotherapy.
2011;45:1433– 38.
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37.
HYPERKALEMIA/ HYPOKALEMIA
Stephen F. Dierdorf
CLINICAL CASE#1
A 16- year- old, 90- kg male was scheduled to undergo an
orchiopexy with general anesthesia. He had not received
general anesthesia in the past and there was no history of
diculty with anesthesia in his immediate family. He was
very afraid of needle sticks and insisted on an inhalation
induction. Vital signs in the preoperative unit were:heart
rate 94 beats per minute; blood pressure 122/ 74mmHg;
respiratory rate 16 breaths per minute; pulse oximetry 99%;
and oral temperature 36.8 degrees C.e plan for general
anesthesia included an inhalation induction with oxygen in
sevourane and airway management with a laryngeal mask
airway (LMA). Ten minutes aer the induction of anesthesia and immediately prior to insertion of the LMA, the
patient developed peaked T waves on the EKG. Soon aer,
premature ventricular contractions developed that progressed to ventricular tachycardia.
PATHOPHYSIOLOGY
Potassium has a central role in a large number of physiologic
functions including blood pressure control, hormone action,
glucose metabolism, and renal and gastrointestinal function.
Potassium plays an important role within the cell by regulating cell volume and protein synthesis, and maintaining
intracellular pH. No functions, however, are more important
than the eects of potassium on cardiac and neuronal electrical activity. Ninety- eight percent of the body’s potassium is
intracellular, and only 2% is extracellular. e concentration
of potassium in the blood is normally maintained between
3.5 and 5.0mmol/ L. Extracellular potassium is actively trans-
ported against this gradient into the cell by the pumping
mechanism of sodium- potassium adenosine triphosphatase.
e impact of the ingestion of large quantities of potassium is
blunted by the uptake of potassium in the liver and muscles,
as well as renal excretion of excess potassium.
1
Potassium movement across cardiac cell membranes
aects depolarization, repolarization, and automaticity.
CLINICAL CASE#2
Alterations in transmembrane potassium concentrations
increase the likelihood of cardiac dysrhythmias, particularly
A 67- year- old 98- kg male was scheduled for an exploratory laparotomy and possible colon resection for a malignant colon tumor. His past medical history was signicant
for hypertension and an inferior wall myocardial infarction (MI) at age 62. Since recovering from his MI, he
those originating in the ventricles. ere are many types of
cardiac ion channels that are encoded by a large number of
genes. It is this potential for genetic variability that is most
likely responsible for the diverse clinical manifestations of
abnormalities in potassium control.
2
walks regularly and has no chest pain with moderate exertion. His medications include atenolol 50 mg daily and
hydrochlorothiazide 50 mg daily. His 12- lead EKG shows
a Q wave in the inferior leads, but it is otherwise normal. Preoperative laboratory values are:hemoglobin 14.2
grams/ dL; sodium 136 mmol/ L; potassium 3.0 mmol/
MECHANISM
Hyperkalemia is less well tolerated than hypokalemia.
Asmall increase in extracellular potassium causes a signi-
cant change in the resting membrane potential of acell.
L; chloride 105 mmol/ L; and bicarbonate 25mmol/ L.
Although there was some concern about the low potassium level, it had been stable and the anesthesiologist felt
the case could proceed, since resection of a malignant
colon tumor was of some urgency.
Hyperkalemia
ere are three dierent ways that plasma potassium
increases: excess intake (oral or intravenous), decreased
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cell, gastrointestinal losses, and excessive renal excretion.
BOX 37.1 DRUGS THAT INCREASE THESERUM POTASSIUM
CONCENTRATION
Angiotensin- converting enzyme inhibitors(ACE)
Movement of potassium into the cell is facilitated by insulin, alkalosis, beta- adrenergic agonists, and xanthines (e.g.,
caeine, theophylline). Chronic diarrhea caused by laxative abuse, celiac disease, and secreting adenomas increase
Angiotensin receptor blockers(ARB)
Beta- adrenergic blockers
potassium loss via the gastrointestinal tract. Impaired bicarbonate reabsorption caused by renal tubular acidosis leads
to increased renal loss of potassium and hypokalemia. Of
Potassium- sparing diuretics (triamterene)
Aldosterone antagonists (spironolactone)
Antibiotics (penicillinG)
Nonsteroidal anti- inammatory drugs (NSAIDs)
note, hypomagnesemia oen occurs in association with
hypokalemia, and one cannot be corrected without correcting the other.
4
In modern clinical practice, the most likely cause of
hypokalemia is chronic administration of diuretics. Athiazide diuretic (hydrochlorothiazide) is one of the front- line
Mannitol
Succinylcholine
drugs for the treatment of hypertension. iazide diuretics
reduce sodium and chloride reabsorption at the distal convoluted tubule. In the collecting ducts, sodium is exchanged
Epsilon- aminocaproicacid
for potassium, resulting in a net loss of potassium. Loop
diuretics such as furosemide reduce sodium, potassium, and
chloride reabsorption in the ascending loop of Henle. e
excretion (renal dysfunction), and shi of potassium from
the intracellular compartment to the extracellular compartment. Inadvertent administration of intravenous potassium
increased delivery of sodium to the distal tubule results in
the exchange of potassium for sodium and accelerated loss
of potassium in the urine.
5
is more likely to cause hyperkalemia than excessive oral
intake of potassium. Metabolically, decreased potassium
excretion due to renal dysfunction and transcellular shi
of potassium are the usual causes of hyperkalemia. Drugs
that interfere with potassium excretion include angiotensin
converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), spironolactone, and beta- adrenergic
blockers. Transcellular shi of potassium can be induced
by beta- adrenergic blockers, mannitol, and succinylcholine
(Box 37.1).
3
Patients with neuromuscular diseases such as spinal
cord injury, burn injury, massive trauma, and muscular
dystrophy are especially susceptible to massive release of
potassium from muscle when exposed to succinylcholine.
Patients with primary myopathies (muscular dystrophy)
have abnormal, weak muscle membranes and up- regulation
of acetylcholine receptors. Succinylcholine and/ or inhaled,
halogenated anesthetics can increase the permeability of the
cell membrane, thereby causing a massive release of intracellular contents including potassium.
RISK OFHYPERKALEMIA
Chronic hyperkalemia is most commonly encountered in
patients with chronic renal disease. Patients with chronic
renal disease have a compensatory increase in aldosterone secretion that increases potassium excretion in their
remaining functioning nephrons. Factors that impair aldosterone excretion or further reduce renal function such as
hypovolemia or infection may lead to acute kidney injury
and clinically signicant hyperkalemia. e risk of hyperkalemia in patients with chronic renal disease is increased
in patients older than 70years of age, patients with diabetes
mellitus, use of ACE inhibitors, and heart failure.
6
Acute, severe, transmembrane release of intracellular
potassium into the blood with serum potassium levels of 12
to 15mmol/ L is characteristic of patients with a primary
myopathy (e.g., muscular dystrophy) and some types of
neurologic diseases. ese patients oen present for surgery before the diagnosis of their underlying pathology is
known. Hyperkalemia of this magnitude progresses rapidly,
Hypokalemia
Hypokalemia is more common than hyperkalemia and
is subclinical in many patients. e causes of hypokalemia include transcellular shi of potassium into the
and the eects on the EKG are profound. Changes in the
EKG begin with peaked T waves, followed by prolongation of the P- R interval, widening of the QRS complex,
ventricular tachycardia, ventricular brillation, and asystole
(Figure 37.1, Box37.2).
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Figure37.1 Tall symmetric peaked T waves characteristic
of hyperkalemia. SOURCE:From Somers MP, Brady WJ, Perron
AD, Mattu A.The prominent T wave:electrocardiographic differential
diagnosis. American Journal of Emergency Medicine. 2002;20:243–
51. With permission.
Risk ofHypokalemia
Most patients tolerate mild hypokalemia with few overt
clinical manifestations. If the hypokalemia develops slowly,
most patients do not have symptoms until the serum potassium level is less than 2.5mmol/ L. Hypokalemia causes
hyperpolarization of the cell membrane, thereby reducing
cell excitability. Muscle weakness, consequently, is one of
the symptoms of hypokalemia. Severe hypokalemia (less
than 2.0mmol/ L) can cause myopathy, respiratory failure,
and rhabdomyolysis.
Typical EKG changes caused by hypokalemia include
ST depression, T wave attening, and increased prominence of the U wave. ese changes are sometimes mistaken
for myocardial ischemia. Cardiac dysrhythmias caused by
hypokalemia include premature ventricular contractions,
supraventricular tachycardia and ventricular tachycardia
(Box37.2).
BOX 37.2 EKG ABNORMALITIES CAUSED BYCHANGES
INPOTASSIUMLEVELS
Hyperkalemia
Peaked Twaves
Prolonged P- R interval
Widened QRS complex
Ventricular tachycardia
Ventricular brillation
Hypokalemia can interfere with the kidney’s ability to
concentrate urine and produces a nephropathy with polyuria and polydipsia. Serum potassium also helps regulate
insulin secretion, and hypokalemia may cause increases in
blood glucose levels.
ASSESSMENT OFTHE PATIENT
7
e only certain method of diagnosing hypokalemia or
hyperkalemia is to measure the potassium level in the blood.
Signs and symptoms of aberrations in potassium homeostasis are oen nonspecic.
Asystole
Hypokalemia
ST segment depression
T wave attening
ProminentUwave
Premature ventricular contractions(PVCs)
Supraventricular tachycardia(SVT)
Ventricular tachycardia
HYPERKALEMIA/HYPOKALEMIA 263
Clinical Case #1 (Hyperkalemia)
e rapidity with which the ventricular tachycardia developed precluded a thorough assessment of the patient. e
EKG changes that developed were classic for severe hyperkalemia. A blood sample for measurement of potassium
should be obtained as quickly as possible. Treatment, however, should not be delayed in order to obtain the sample.
e serum potassium in this case was 11mmol/ L. is clinical scenario suggests that the patient had an undiagnosed
myopathy, most likely muscular dystrophy. Acreatine kinase
level obtained soon aer resuscitation was >50,000IU.
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Clinical Case #2 (Hypokalemia)
An elderly adult with a history of hypertension who is
receiving a thiazide diuretic (hydrochlorothiazide) should
raise the suspicion of hypokalemia. e measurement of
serum electrolytes prior to induction of anesthesia was
degeneration and regeneration in patients with DMD and
BMD is complex, and the potential for rhabdomyolysis is
dicult to predict. Most agree that succinylcholine should
be avoided in patients with muscular dystrophy, but the
best choice of other anesthetics is controversial.
8
clearly indicated. Amagnesium level should also be measured. e patient should be carefully questioned about any
history of muscle weakness or palpitations.
MANAGEMENT OFHYPOKALEMIA
(CLINICALCASE#2)
MANAGEMENT OFHYPERKALEMIA (CLINICAL
CASE#1)
Mild hypokalemia is dened as serum potassium between
3.0 and 3.5 mmol/ L. Moderate hypokalemia is dened
as serum potassium between 2.5 and 3.0mmol/ L. Severe
e types of patients that typically develop acute hyperkalemia during anesthesia are (1)renal patients with chronic
hyperkalemia that have a further increase in potassium
during surgery; (2) patients with acute rhabdomyolysis;
and (3) patients with rapid, massive transfusion of old
banked blood rich in potassium secondary to hemolysis.
Hyperkalemia from massive transfusion generally occurs in
infants and small children and only rarely in adults. It is prudent to preoperatively measure serum potassium in patients
with chronic renal disease. e precise level of potassium
at which there is an increased risk of signicant intraoperative hyperkalemia is not well dened. Aserum potassium
of 6.0mmol/ L or higher would warrant consideration for
delaying surgery that is not emergent. e administration of
succinylcholine elevates serum potassium 0.5 to 0.7mmol/
L. A patient with a preexisting serum potassium of 6 to
6.5mmol/ L could develop symptomatic hyperkalemia aer
succinylcholine administration.
Intraoperative rhabdomyolysis that causes severe hyper-
kalemia (9 to 15 mmol/ L) typically occurs in patients
hypokalemia is considered to be less than 2.5mmol/ L. Mild
hypokalemia is very common, and most patients are asymptomatic. ree decades ago, any preoperative potassium less
than 3.5mmol/ L frequently resulted in the postponement
of elective surgery. ere was concern that respiratory alkalosis secondary to hyperventilation might cause an intracellular shi of potassium and a further decrease in serum
potassium. e recommendation, therefore, was to maintain normocarbia especially in patients receiving digitalis.
is arbitrary recommendation has since been challenged,
and it was discovered that most patients did not have perioperative complications secondary to mild hypokalemia.
e primary concern in patients with hypokalemia is
the risk of ventricular dysrhythmias. Hypokalemia prolongs
the cardiac action potential and decreases the refractory
period, thereby increasing the risk of reentrant ventricular dysrhythmias. Most studies of cardiac dysrhythmias in
surgical patients with mild to moderate hypokalemia, however, have not shown a signicant increase in the risk of
intraoperative dysrhythmias.
9
with a primary myopathy. Duchenne muscular dystrophy
(DMD) and Becker muscular dystrophy (BMD) are Xlinked dystrophinopathies. Dystrophin is a large protein
located on the cytoplasmic side of the muscle membrane.
Dystrophin helps maintain the structural integrity of the
muscle membrane. e DMD patients lack dystrophin and
BMD patients have insucient quantities of dystrophin or
abnormal dystrophin. Any stimulus (e.g., succinylcholine)
can disrupt the muscle membrane and release large quantities of potassium into the circulation. Inhaled, halogenated
anesthetics have also been reported to cause rhabdomyolysis and hyperkalemia. Although intravenous agents seem
less likely to cause rhabdomyolysis, there have been reports
of rhabdomyolysis aer exposure to intravenous anesthetics. Every patient with muscular dystrophy, however,
does not develop rhabdomyolysis. e process of muscle
TREATMENT OFHYPERKALEMIA
Treatment of hyperkalemia can be divided into three
phases depending on the rapidity with which treatment is
required (Box 37.3). e most eective immediate treatment for acute, severe hyperkalemia is the administration
of calcium gluconate (20– 30 mg/ kg). is is the initial
treatment of choice for severe hyperkalemia in the surgical patient. Calcium is eective within seconds to minutes.
Although the precise mechanism for the ecacy of calcium
is not known, it most likely restores the transmembrane
potential of cardiac cells. Calcium does not, however, aect
the potassium concentration in the blood. Calcium gluconate is the preferred preparation for administration via a
peripheral vein as calcium gluconate is less likely to cause
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a temporary decrease in serum potassium in exchange for
BOX 37.3 THERAPEUTIC MODALITIES FORHYPERKALEMIA
RapidOnset
intracellular hydrogenions.
Oral or rectal administration of polystyrene sulfonate
resin binds potassium in the colon and promotes potassium
(1– 2 minutes)
Calcium gluconate (20 to 30 mg/ kgIV)
excretion. is method requires 10 hours, and the eect is
unpredictable.
10
or Calcium chloride (10 to 20 mg/ kgIV)
Treatment ofHypokalemia
Discontinue potassium- containinguids
e indications for the treatment of hypokalemia are not
Hyperventilate with 100%oxygen
IntermediateOnset
well dened. e rst issue to resolve is whether the hypokalemia is adversely aecting the patient. A search for
other metabolic abnormalities such as hypomagnesemia or
(15– 30 minutes)
Insulin (10 units IV) + dextrose (0.25 g/ kgIV)
metabolic alkalosis that may contribute to hypokalemia is
warranted.
It is best not to treat a surgical patient with hypokalemia
Inhalation of albuterol (20mg)
Sodium bicarbonate (1– 2 mEq/ kg)
if there is no evidence that it is causing an adverse eect. If
it is felt that the surgical patient with hypokalemia requires
the intravenous administration of potassium, it must be
Furosemide (15mgIV)
done very cautiously. Rapid administration of intravenous
potassium can alter the transmembrane electrical gradient
LateOnset
(Hours)
and provoke cardiac dysrhythmias. e intravenous administration of potassium to an adult patient should not exceed
20 mEq per hour. A useful guideline for the administra-
polystyrene sulfonateresin
(13– 30 grams rectally)
tion of potassium during surgery is to administer 1 mEq
of KCL for each liter of the patient’s blood volume. For
example, the administration of 5 mEq of KCl to an adult
Consider dialysis or extracorporeal membrane
oxygenation(ECMO)
with a 5 liter blood volume would not increase the potassium by more than 1mmol/ L. In practice, it is very unlikely
to increase it that much, as potassium will diuse into the
interstitialspace.
tissue necrosis if subcutaneous inltration occurs. Calcium
chloride is ideally administered through a central venous
catheter.
Insulin increases potassium uptake by muscle cells and
decreases the plasma potassium concentration by shiing
potassium from the blood into the cells. Insulin is eective
within 15 minutes. e administration of dextrose with
insulin enhances the potassium shi and reduces the risk
of hypoglycemia.
Inhalation of albuterol, a beta2- adrenergic agonist,
shis potassium intracellularly by activating the sodiumpotassium pump via a mechanism dierent from that of
insulin. Furosemide increases potassium excretion via the
kidneys within 2 to 4 hours. Furosemide, however, may
be of minimal value in patients with chronic renal disease. Hemodialysis may be required to lower serum potassium levels in patients with severe chronic renal disease.
Administration of sodium bicarbonate has been recommended in an attempt to alkalinize the blood and cause
FOLLOW- UP OFHYPERKALEMIA (CLINICAL
CASE#1)
e EKG ndings were typical of acute severe hyperkalemia. e patient immediately received 30 mg/ kg of calcium gluconate through his peripheral IV and received one
countershock. His cardiac rhythm converted to sinus. As
the serum potassium was 11mmol/ L, he was given 10 units
of regular insulin and 12.5 grams of dextrose intravenously.
An arterial catheter was inserted into his right radial artery
to facilitate frequent measurements of potassium and creatine kinase. His cardiac rhythm remained stable, and his
serum potassium 2 hours later was 5.3 mmol/ L. He was
transferred to the ICU for continual monitoring and serial
measurement of metabolic parameters. He remained stable
for 24 hours and was transferred to the ward. He complained of muscle soreness for 72 hours aer the episode.
His creatine kinase level decreased to 3,500 aer 72 hours,
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