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propranolol. erapy with beta- adrenergic blockers
REFERENCES
must, however, be closely monitored, as heart failure
can develop in susceptible patients. Hydrocortisone
should also be administered as soon as the diagnosis of
thyrotoxicosis is suspected. yroid hormone increases
the degradation of glucocorticoids, and hyperthyroid
patients have a functional adrenal insuciency.
4. What laboratory tests should be performed to ensure
that a hyperthyroid patient is euthyroid prior to elective
surgery? e hyperthyroid patient should be rendered
euthyroid prior to elective surgery. Hyperthyroid
patients have a low TSH level as the thyroid hormone
suppresses TSH production. In most cases, the best
measure of a return of normal thyroid function is a
normal TSH level. It is also important that the patient
be clinically euthyroid. ere are cases where the TSH
level is normal, but thyroid hormone production
is still increased. e resting heart rate and blood
pressure should be normal, and the patient’s other
manifestations of hyperthyroidism should have abated
1. Devereaux D, Tewelde SZ. Hyperthyroidism and thyrotoxicosis.
Emergency Medicine Clinics of North America. 2014;32:277– 92.
2. Muldoon BT, Mai VQ, Burch HB: Management of Graves’ disease. Endocrinology and Metabolism Clinics of North America.
2014;43:495– 516.
3. Franklyn JA, Boelaert K. yrotoxicosis. Lancet. 2012:379:1155– 66.
4. Burgi H. Iodine excess. Best Practice & Research Clinical
Endocrinology & Metabolism. 2010;24:107– 15.
5. Laliberte BD, Goldenberg E, Reece- Stremtan SJ. Intraoperative
diagnosis and treatment of thyroid storm in a 15- year- old male.
A&A Case Reports. 2014;3:107– 9.
6. Biondi B, Kahaly GJ. Cardiovascular involvement in patients with
dierent causes of hyperthyroidism. Nature Reviews Endocrinology.
2010;6:431– 43.
7. Langley RW, Burch HB. Perioperative management of the thyrotoxic patient. Endocrinology and Metabolism Clinics of North
America. 2003;32:519– 34.
8. Shindo M. Surgery for hyperthyroidism. Journal for
Otorhinolaryngology and Its Related Specialties.
2008;70(5):298– 304.
9. Nayak B, Burman K. yrotoxicosis and thyroid storm.
Endocrinology and Metabolism Clinics of North America.
2006;35:663– 86.
10. Klubo- Gwiezdzinska J, Wartofsky L. yroid emergencies. Medical
Clinics of North America. 2012;96:385– 403.
aer antithyroid therapy.
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35.
MYXEDEMACOMA
Jacquelyn E. Allison and Julie D.Dunlap
CLINICALCASE
levels of T3 can lead to profound hypothermia (<27 degrees
C) and depressed cardiac activity (Figure 35.1). Suppressed
A 74- year- old, 71- kilogram female with a 6- month history
of intermittent abdominal pain and nausea was referred
to the general surgical service aer ultrasound of the gallbladder identied several large gallstones. e patient had
a recent weight gain of 10kg and was hypothermic with a
temperature of 35.8 degrees Celsius in the preoperative care
unit. Induction of anesthesia and tracheal intubation were
uneventful. Soon aer induction, blood pressure decreased
from 130mmHg systolic to 80mmHg systolic. Ephedrine
(10 mg) and phenylephrine (50 micrograms) increased
blood pressure to 95mmHg systolic. At the conclusion of
surgery, the patient was extubated and transported to the
postanesthesia care unit (PACU). Vital signs in the PACU
were:heart rate 62 beats per minute, blood pressure 136/
87mmHg, respiratory rate 8 breaths per minute. She was
lethargic, and deep tendon reexes were absent.
cardiac function presents as decreased inotropism and chro-
notropism with vasoconstriction. Neurovascular adaptions
include: peripheral vasoconstriction, diastolic hyperten-
sion, and diminished blood volume.2 In the decompensated
state, low cardiac output and hypotension will result in car-
diogenic shock that may or may not be responsive to vaso-
pressors without thyroid hormone replacement.
3
Decreased central nervous system sensitivity to hypoxia
and hypercapnia leads to respiratory failure.4 Other factors
that contribute to respiratory compromise include skeletal
muscle dysfunction, obesity, pleural eusions, macroglossia, infection, and aspiration.
Increased vascular permeability leads to eusions and
total body edema. Renal function is decreased, resulting in hyponatremia and uid retention. Hypoglycemia,
depressed cerebral function, hyponatremia, hypoxemia,
and reduced cerebral blood ow decrease the level of con-
PATHOPHYSIOLOGY
Regulation of thyroid function is a feedback system composed of the hypothalamus, the pituitary gland, and the
thyroid gland. yrotropin- releasing hormone (TRH)
secreted by the hypothalamus stimulates release of thyroidstimulating hormone (TSH) by the pituitary. e TSH in
turn causes release of thyroxine (T4) by the thyroid. T4 is
deiodinated in the liver and kidneys to T3, which subsequently increases metabolism and the physiologic responses
needed to meet increased metabolic demand.
sciousness (Table35.1).
RISK
Myxedema coma is rare, with an incidence of 0.22 per million per year. Hypothyroidism is eight times more common in women than men, and typically presents in the
later decades of life. Eighty percent of cases of myxedema
occur in women over 60years. It most oen aects hospitalized elderly women with long- standing, undiagnosed
hypothyroidism.
5
Myxedema oen presents in patients who develop a systemic illness such as pneumonia, urinary infection, conges-
MECHANISM
Myxedema coma presents as a life- threatening form of severe
hypothyroidism. e typical patient presents with severe
biochemical hypothyroidism, including an elevated serum
TSH level and decreased T3 and T4 levels.1 Inadequate
tive heart failure, or a cerebrovascular event superimposed
on previously undiagnosed hypothyroidism. ere may be
a history of thyroid disease or discontinuation of thyroid
treatment. Apituitary or hypothalamic basis for hypothyroidism can be elicited in 5%– 10% of patients. Patients with
myxedema coma typically present in the winter months,
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Hypothyroidsm and precipitating factor
Low serum T4 and intracellular T3
Fluid retention
Figure35.1 Pathogenesis of myxedema coma. SOURCE:Adapted from Mathew V, Misgar R, Ghosh S, etal. Myxedema coma:a new look into an old crisis. Journal of Thyroid
Research. 2011, Article ID 493462,1–7.
TABLE35.1 CLINICAL AND LABORATORY FEATURES
OFMYXEDEMACOMA
Cardiovascular Neuropsychiatric
Bradycardia and hypotension
Cardiomegaly
Low cardiacoutput
Pericardial effusion
Cardiogenicshock
Bundle branch blocks and
arrhythmias
Nonspecic ECG ndings
Respiratory Renal and water metabolism
Hypotaxia
Hypercarbia
Myxedema oflarynx
Pleural effusion
Pneumonia (precipitating
factor)
Gastrointestinal Metabolic
Anorexia and nausea
Abdominalpain
Constipation
Paralyticileus
Toxic megacolon
Gastricatony
Neurogenic oropharyngeal
dysphagia
SOURCE:Adapted from Mathew V, Misgar R, Ghosh S, etal. Myxedema coma:a new look
into an old crisis. J Thyroid Res. 2011, Article ID 493462,1– 7.
Decreased inotropism and chronotropism Hypothermia Stupor
Hyponatremia Cardiogenic shockRespiratory failure
COMA
association with certain drugs including anesthetics, sedatives, opioids, amiodarone, and antineoplastic drugs (tyrosine kinase inhibitors) (Box35.1).
Confusion and obtundation
Lethargy
Coma
Seizures
Poor cognitive function
Depression and Psychosis
ASSESSMENT OFTHE PATIENT
Patients with myxedema coma may present with altered
mental status, hypothermia, or an absence of fever despite
a systemic infection. Physical examination may reveal features of hypothyroidism like dry skin, coarse hair, a hoarse
voice, hypothermia, delayed deep tendon reexes, edema,
Fluid retention
Anasarca
Hyponatremia
Bladderatony
Urine sodium normal or increased
Urine osmolality > serum osmolality
and goiter. Hypothermia can be profound and is oen the
rst clinical clue to the diagnosis.
Typical cardiovascular ndings in myxedema coma
include nonspecic electrocardiographic abnormalities,
cardiomegaly, bradycardia, prolonged QT interval (may
progress to torsades de pointes), and reduced contractility.7
Severe hypoxia and hypercarbia are secondary to respira-
Hypothermia
Hypoglycemia
tory depression.
Given a reasonable index of suspicion, a probable diagnosis of myxedema coma can be made with the history,
physical ndings, and thyroid function tests (e.g., elevated
TSH level) showing hypothyroidism. Hyponatremia, metabolic acidosis, and elevated levels of creatine phosphokinase and lactate dehydrogenase can alsooccur.
Worsening mental status
suggesting that external cold may be a factor.6 ere are
case reports of myxedema coma induced by chronic ingestion of large amounts of raw bok choy, which can lead to
an underproduction of thyroid hormone.7 ere is also an
248 SECTION B. ENDOCRINE DISTURBANCES
CONSIDERATIONS FORANESTHESIA
Elective surgery should be postponed in patients diagnosed with severe hypothyroidism or myxedema. e usual
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as a result of anesthetic- induced vasodilation in a patient
BOX 35.1 PRECIPITANTS OFMYXEDEMA
with pre- existing uid depletion. e response to vasoactive drugs may be extremelypoor.
Discontinuation ofthyroid replacement medications
DRUGS
Antineoplasticagents
Lithium
TREATMENT
Mortality in untreated myxedema coma is nearly 100%.
Even with optimum therapy a mortality rate as high as 30%–
60% has been reported.8 Because of this and the need for
Amiodarone
Opioids
multimodal treatment, patients with myxedema should be
admitted to the intensive care unit (ICU) for continuous
monitoring and care. Mechanical ventilation is oen required
Anxiolytics
Excessive ingestion of bokchoy
due to both hypoventilation and coma. Arterial blood gases
are useful to guide ventilation and acid/ base status.
External warming of the patient is necessary but should
INFECTION
Pneumonia
be done with caution, due to the risk of hypotension associated with vasodilation; therefore intravenous volume
repletion should be performed prior to external warming.
Urinarytract
Sepsis
Vasopressors may be required to maintain blood pressure.
Treatment with thyroid hormone may increase cortisol clearance and precipitate adrenal insuciency. Steroids should,
Congestive heart failure
Stroke
therefore, be administered.7 Hydrocortisone (1 mg/kg)
is a good choice for initial corticosteroid replacement.
yroid hormone is the mainstay of treatment for
Hypothermia
Electrolyte abnormalities
patients with myxedema coma; however, the regimen by
which to do so remains controversial (Box 35.2). e main
considerations with oral thyroid replacement therapy are
Hypoglycemia
Hyponatremia
the absorption and distribution of the administered hormone and onset of action.2 Parenteral preparations of T3
and T4 are readily available and should be used for lethargic
Acidosis
or comatose patients. T4 must be converted to T3 before an
appreciable metabolic eect develops. e onset of action
presentation for the anesthesiologist, however, is a patient
with unknown hypothyroidism that progresses to myxedema during surgery and the immediate postoperative
period. Manifestations of severe hypothyroidism during
the perioperative period may include reduced cardiac output, hypotension, hypoxemia, hypercapnia, upper airway
obstruction, and altered mental status. ese eects are not
unique to hypothyroidism, but myxedema must be considered in the dierential diagnosis of patients with such a
clinical presentation.
Upper airway obstruction is common and is second-
ary to swelling of so tissues in the upper airway and
of T4 is consequently, slower. T3 is rapid in onset, but introduces the risk of increasing metabolism before the heart can
increase function and cardiac output to meet the increased
metabolic demand. is patient was treated with both T3
and T4 due to the severity of the hypothyroidism.
9
In the PACU, the patient developed signicant upper
airway obstruction and required tracheal intubation.
yroid function studies showed a markedly elevated TSH
level and low T3 and T4 levels; 250 micrograms of T4 and
10 micrograms of T3 were administered intravenously.
Hydrocortisone (100 mg) was also administered. e
patient was transferred to theICU.
skeletal muscle dysfunction. Airway obstruction in combination with poor ventilatory responses to hypoxia and
hypercapnia are strong indications for tracheal intubation
and controlled ventilation for most surgical procedures.
Hypotension aer exposure to anesthetics is very common
FOLLOW- UP
Intravenous therapy with T3, T4, and hydrocortisone was continued in the ICU. Her level of consciousness increased, and
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the critical factor is the physician’s index of suspicion
BOX 35.2 INTRAVENOUS THYROID HORMONE
REPLACEMENT FORSEVERE HYPOTHYROIDISM
Therapy Usually with T4orT3
T4 + T3 May Be Required for MyxedemaComa
Levothyroxine(T4)
Loading dose:1.6 micrograms/ kg:rst 24hours
1 microgram/ kg/ 24 hours until oral therapybegins
T3
Loading dose:10– 20 micrograms
10 micrograms every 4 hours for rst 24hours
10 micrograms every 6 hours for days 2and3
If T4 + T3 Required
T4:Load with 4 micrograms/ kg
100 micrograms onday2
that leads to the laboratory diagnosis.
2. When the diagnosis of myxedema coma was suspected
in the PACU, what additional monitors or lines
should have been considered for continued care of this
patient? An intra- arterial catheter would be extremely
useful for continuous blood pressure monitoring and
frequent blood sampling for measurement of arterial
blood gases, electrolytes, and glucose. Atransthoracic
echo (TTE) could provide important information
about ventricular function during the treatment
process. It is important that cardiac function increase
at a pace needed to meet the increased metabolic
demands of thyroid hormone replacement. If there is
coexisting arteriosclerotic heart disease (quite likely
in this elderly patient), a rapid increase in metabolic
demand can exceed the heart’s ability to increase
cardiac output.
50 micrograms onday3
T3:10 micrograms every 8hours
Corticosteroids
Hydrocortisone 100 mg every 8hours
3. If the diagnosis of myxedema coma was initially made
intraoperatively what would have been the plan for
postoperative airway management? Consideration of
all the factors aecting this patient may well lead to the
conclusion that controlled postoperative ventilation
in the ICU would be best. Clearance of any drugs that
she was extubated 48 hours aer surgery. Aer she was able to
ingest oral uids, oral thyroid replacement therapy was instituted. She was subsequently referred to an endocrinologist for
regulation of her long- term thyroid replacement therapy.
Although myxedema is relatively rare, this case represents a common mode of presentation. e anesthesiologist
must consider myxedema in any patient that exhibits a deterioration in mental status aer surgery.
10
can produce respiratory depression and neuromuscular
blockers is unpredictable, and postoperative respiratory
failure could result. e potential for a mismatch of
metabolic demand and cardiac output precipitating
cardiac failure during thyroid hormone replacement
would also support the indication for postoperative
controlled ventilation.
4. How should thyroid hormone replacement be
initiated? yroid hormone replacement should begin
with levothyroxine (1.6 mcg/ kg/ 24 hr). Levothyroxine
CASE- BASED LEARNING DISCUSSION
is synthetic T4 that is converted to T3 in the same
manner that endogenous T4 is converted to T3. e
1. Should the possibility of myxedema coma have been
considered during the initial evaluation of this patient?
e progressive development of hypothyroidism
leading to myxedema is usually insidious and dicult
for patients and their family members to recognize. e
recent weight gain and the preoperative hypothermia
are the best clues to thyroid dysfunction. However it
is unlikely that these two ndings would have aroused
signicant suspicion of hypothyroidism. Although the
laboratory diagnosis of hypothyroidism is very reliable,
dose of levothyroxine should be reduced for this elderly
patient until an adequate increase in cardiac function is
achieved. When the hypothyroidism is as severe as that
of this patient, administration of T3 may be necessary.
Once it has been determined that an acceptable balance
between increased metabolic rate and cardiac function
has been achieved, the patient can be extubated.
Aeuthyroid state may require several weeks of
adjustment of the levothyroxine dose based on repeated
TSH levels.
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REFERENCES
6. Dutta P, Bhansali A, Mascodi SR, Bhadada S, Sharma N, Rajpu R.
Predictors of outcome in myxedema coma:a study from a tertiary
1. Mallipedhi A, Vali H, Okosieme O. Myxedema coma in a patient
with subclinical hypothyroidism. yroid. 2011;21:87– 89.
2. Mathew V, Misgar R, Ghosh S, etal. Myxedema coma:a new look
into an old crisis. Journal of yroid Research. 2011; Article ID
493462,1– 7.
3. Klein I, Ojamaa K. yroid hormone and the cardiovascular system.
New England Journal of Medicine. 2001;344:501– 9.
4. Ladenson PW, Goldenheim PD, Ridgeway EC. Prediction and
reversal of blunted ventilatory responsiveness in patients with hypothyroidism. American Journal of Medicine. 1988;84:877– 83.
5. Klubo- Gwiezdinska J, Wartofsky L. yroid emergencies. Medical
care centre. Critical Care. 2008;12:1– 8.
7. Wartofsky L. Myxedema coma. Endocrinology and Metabolism
Clinics of North America. 2006;35:687– 98.
8. Dubbs SB, Spangler R. Hypothyroidism. Emergency Medicine
Clinics of North America. 2014;32:303– 317.
9. Biondi B, Wartofsky L. Combination therapy with T4 and T3:toward
personalized replacement therapy in hypothyroidism? Journal of
Clinical Endocrinology and Metabolism. 2012;97:2256– 71.
10. Chiong YV, Bammerlin E, Mariash CN. Development of an
objective tool for the diagnosis of myxedema coma. Translational
Research. 2015;166:233– 43.
Clinics of North America. 2012;96:385– 403.
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36.
ACUTE LIVER FAILURE
Cynthia Wang and Michelle Y. Braunfeld
CLINICALCASE
bilirubin levels and high aminotransferase levels. Drug over-
dose and viral hepatitis typically result in acute liver failure,
A 20- year- old female presented to the emergency department (ED) with acute changes in her mental status. She had
been found semiconscious in her parents’ backyard and was
rushed to the ED. Her past medical history was signicant
for depression, for which she was taking a serotonin reuptake inhibitor. She had been taking several over- the- counter
which has a latency period of 1 to 4 weeks. Subacute cases of
liver failure evolve over 6months and are usually secondary
to drug- induced liver injury. e more gradual progression
of liver dysfunction in subacute cases is associated with lower
serum aminotransferase levels and higher bilirubin levels.
Patients with subacute liver failure have a poorer prognosis.
analgesics for the recent onset of lower back pain. Vital signs
in the ED were: heart rate 143 beats per minute; blood pressure 81/ 35 mmHg, respiratory rate 42 breaths per minute.
Arterial oxygen saturation (pulse oximeter) was 93%. She
is receiving oxygen by facemask (FiO2 = 0.45). Laboratory
results from the ED: arterial pH 6.97, acetaminophen level
of 215 mcg/ mL, INR > 10, and factor V activity level of
5%. Her ammonia level was 116 micromol/ L. Urine output
was minimal and continuous venovenous hemoltration
was initiated. An initial cranial CT was normal. Twentyfour hours aer admission, a repeat cranial CT showed signicant cerebral edema. Neurosurgery was consulted for
placement of an intracranial pressure monitor.
ETIOLOGY
In developed countries, the incidence of viral- induced
acute liver failure has decreased, while the incidence of
drug- induced liver failure has increased. Acetaminophen
toxicity is the most common cause of drug- induced liver
failure in the United States. Toxicity usually occurs from
careless ingestion of multiple acetaminophen- containing
products and is enhanced by chronic use of alcohol. Non-
acetaminophen- induced acute liver failure has been attrib-
uted to anticonvulsants, anti- inammatory drugs, and
herbal medications (Figure 36.1, Table 36.1). Although
only 10% of patients with drug- induced liver injury prog-
PATHOPHYSIOLOGY
Acute liver failure is characterized by the sudden impairment of liver function accompanied by encephalopathy and
coagulation defects in a patient without preexisting liver
disease. Liver tissue histology shows massive hepatocellular
necrosis. Dierent etiologies have dierent latency periods
with regard to time of onset and appearance of liver failure.
Although the terms “hyperacute,” “acute,” and “subacute”
have been used to characterize disease latency, this classication has no relevance to prognosis, but may have relevance
to etiology. Hyperacute liver failure is oen caused by acetaminophen (paracetamol, N- acetyl- p- aminophenol) toxicity or viral infection, and patients develop encephalopathy
within 1 week of onset. e severe degree of cellular necrosis that occurs with hyperacute failure is reected in the low
ress to acute liver failure, 80% of patients that do develop
acute liver failure either die or require liver transplantation.
Globally, viral infections due to hepatitis A, B, and E
are the most common causes of acute hepatic failure. Acute
liver failure from hepatitis B can also result from reactivation of a chronic disease process. is occurs in patients
with chronic, subclinical hepatitis B who are immunosuppressed. Acute liver failure from hepatitis C is rare. Other
viruses reported to cause acute liver failure include cytomegalovirus, Epstein- Barr virus, human herpes simplex
type 1 and 2, human herpes virus 6, varicella zoster virus,
and parvovirus19.
Less common causes of acute liver failure are mushroom poisoning, Wilson’s disease (copper), autoimmune
hepatitis, and Budd- Chiari syndrome. Acute liver failure
due to fatty liver of pregnancy (HELLP syndrome) usually
resolves aer delivery.
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and inammatory mediators such as interleukin (IL)- 6
Other drugs
40%
Antibiotics
14%
Antiepileptics
18%
and tumor necrosis factor alpha (TNF- α) cause cyto-
toxicity. As the liver fails, astrocytes cannot metabolize
ammonia to urea, but convert it to glutamine. Glutamine
adversely aects mitochondrial function, resulting in
cellular hyperosmolarity. e rapid onset of hyperam-
NSAIDs
4%
Statins
4%
Antituberculosin
20%
monemia overwhelms normal osmotic compensatory
mechanisms, and cerebral edema ensues. Inammatory
mediators (cytokines) increase cerebral endothelial permeability and contribute to vasogenic intracranial hypertension.3 Concomitant systemic infection that produces
Figure36.1 Proportion of non- acetaminophen- induced liver failure in the
United States, 1997– 2006.
MECHANISM
e diverse clinical manifestations of acute liver failure are
secondary to the myriad of metabolic functions of theliver.
a systemic inammatory response may accelerate the progression of encephalopathy (Table36.1).
Cardiovascular Effects
Patients with acute liver failure typically have a high cardiac
output, low systemic vascular resistance, and hypotension.
Initial hypotension is secondary to hypovolemia, although
Neurologic Effects
Encephalopathy is a hallmark of acute liver failure and
adrenal insuciency may also be a contributing factor.
Circulating inammatory mediators may also depress myo-
cardial contractility.
intracranial hypertension secondary to cerebral edema
is the leading cause of death from acute liver failure.2
Although there is evidence for both cytotoxic and vasogenic mechanisms, the evidence for cytotoxicity is more
compelling. Circulating neurotoxins such as ammonia
Coagulopathy
Acute liver failure leads to a rapid reduction in clot-
ting factors, especially factors VII and V. e degree of
TABLE36.1 DRUGS IMPLICATED INNON- ACETAMINOPHEN ACUTE LIVER FAILURE
Antibiotics
nitrofurantoin phenytoin isoniazid ator vastatin diclofenac propylthiouracil
ketoconazole valproate cerivastatin bromfenac disulfuram
amoxicillin and
clavulanate
trimethoprimsulfamethoxazole
minocycline ezetimibe naproxen methotrexate
terbinane uvastatin indomethacin methyldopa
ciprooxacin mercaptopurine
levooxacin azathioprine
telithromycin herbal medications
itraconazole
moxioxacin
Antiepileptics Antituberculosin Statins NSAIDs
carbamazepine simvastatin ibuprofen halothane
felbamate pravastatin etodolac amitriptyline
Other Drugs
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coagulopathy, however, may be out of proportion to the
severity of liver failure. It is not unusual for a patient with
severe hepatic encephalopathy to exhibit only mild to moderate coagulopathy (INR 1.5 to 5). Clotting factor repletion is not recommended unless the INR is > 6.0 or in
to counter the catabolic state that liver failure causes.
Ammonia levels, however, must be frequently measured, as
overzealous protein administration may exacerbate hyperammonemia. Phosphate, magnesium, and potassium levels
are oen decreased and should be monitored.
preparation for an invasive procedure.
Platelet levels and function can also be aected. In
patients with chronic liver disease, thrombocytopenia and
thrombocytopathy are secondary to portal hypertension,
splenic sequestration, and decreased thrombopoietin levels. Patients with acute liver failure, however, typically have
elevated thrombopoietin levels that do not correlate with
platelet counts. Platelet adhesion and activation may be
decreased.
It is important to note that although procoagulant factors are reduced, anticoagulant factors are also reduced.
Antithrombin III levels are low, as are levels of proteins C
and S; therefore patients with acute liver failure may also be
susceptible to thrombotic complications. e coagulopathy
of acute liver failure is complex and can lead to disseminated intravascular coagulation (DIC) and hyperbrinolysis. As a result, whole- blood viscoelastic testing in addition
to conventional coagulation tests (prothombin time, partial prothromoplastin time, international normalized ratio,
platelet count, brinogen levels) may be benecial in assessing a patient’s coagulation status.
RISK
Since acute liver failure adversely aects every system in
the body, complications can manifest in many organs.
e most common cause of mortality in patients with
acute liver failure is cerebral edema. Mortality is greater
than 80% in patients with cerebral edema as opposed to
the 45% seen in patients without cerebral edema. e
decline of hepatic metabolic function leads to hypoglycemia and lactic acidosis. Pulmonary infection is common, and acute lung injury with respiratory distress can
occur. Renal failure occurs in 40% to 80% of patients and
is highest in patients with acetaminophen- induced liver
failure.
Although hepatic failure markedly reduces synthesis of coagulation factors, the concomitant reduction in
antithrombotic factors may balance the coagulopathy.
Gastrointestinal bleeding occurs in up to 20% of patients
with acute liver failure. is is usually a result of stress ulceration of the gastric mucosa rather than coagulopathy.
Renal Effects
Renal dysfunction occurs in 50% of patients with acute
liver failure. It most commonly occurs in elderly patients
and in patients with acute liver failure secondary to acetaminophen toxicity or other agents with direct nephrotoxic
eects. Resolution of the liver failure, however, usually leads
to normalization of renal function. Patients who require
renal replacement therapy are usually started on continuous
rather than intermittent dialysis. is ensures a greater level
of metabolic and hemodynamic stability. Renal replacement therapy is important for reducing ammonia levels,
correcting acidosis, and treating volume overload, all of
which increase the risk of cerebraledema.
ASSESSMENT OFTHE PATIENT
is patient exhibits the typical clinical picture of acute
liver failure in the United States. She is young and in generally good health with no previous history of hepatic
disease. To treat her back pain, she most likely had been
ingesting dierent over- the- counter analgesics, all of
which contained acetaminophen. Her tachycardia and
hypotension reect the vasodilation and hypovolemia
that occurs with liver failure. An echocardiogram may be
indicated as subclinical myocardial dysfunction can occur.
Areduced cardiac output can lead to decreased hepatic
perfusion and further aggravation of the liver injury.
e encephalopathy indicates a very poor prognosis and
requires aggressive therapy to reduce the cerebral edema.
Metabolic Effects
Hypoglycemia is common in patients with acute liver
failure. Coexisting encephalopathy may mask the signs of
hypoglycemia, thus requiring frequent measurement of
blood glucose levels. Enteral feedings should be initiated as
soon as possible. Protein supplementation may be required
Although her coagulation studies are grossly abnormal,
she has no evidence of overt bleeding. Nevertheless,
implantation of an intracranial pressure monitor may
require replacement of coagulation factors. e profound
metabolic acidosis is secondary to reduced hepatic clearance of lactate and hypoperfusion. She is oliguric and may
have renal dysfunction.
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CONSIDERATIONS FORANESTHESIA
e goals for perioperative management are (1) prevention
of further organ damage and (2) treatment of current complications of acute liver failure. e immediate concerns
are (1) encephalopathy, (2) metabolic acidosis, (3) coagulopathy, (4) oliguria/ anuria, (5) metabolic dysfunction, and
(6)respiratory compromise. Invasive monitoring with an
surgery was 1.6. e initial ICP aer implantation of the
monitor was 35mmHg. Mannitol (0.5 g/ kg over 5 minutes) was administered, and ventilation was increased to
lower the PaCO2 to 30mmHg. Aer implantation of the
ICP monitor, she was transferred to the ICU. She remained
intubated, and controlled ventilation was continued. Two
hours aer insertion of the ICP monitor, her ICP was
18mmHg.
arterial catheter is absolutely required. Serial arterial blood
gases, serum electrolytes, glucose, and coagulation studies
will help guide intraoperative management of glycemia,
dyskalemia, and acidosis. Transesophageal echocardiography may be a useful intraoperative monitor of myocardial
contractility and intravascular volume.
Halogenated agents may increase cerebral blood flow
and increase intracranial pressure, and therefore should
be used with caution, if at all. Although controversial,
these agents may cause hepatic dysfunction and aggravate the degree of liver failure. Furthermore, potential
hypotension from halogenated, inhaled anesthetics
can decrease cerebral perfusion pressure and decrease
hepatic and renal blood flow. As a result, total intravenous anesthesia (TIVA) is often considered to be a better choice. Prolonged clearance of intravenous drugs
(opioids, hypnotics) should be anticipated because of
severe liver and renal dysfunction. Cis- atracurium is the
logical choice for muscle relaxation, as its clearance is
minimally affected by hepatic and renal dysfunction. If
immediate weaning and extubation of the patient is not
anticipated, the choice of neuromuscular blocking agent
may not be as pertinent.
Perioperatively, the patient should be placed in a
20- to 30- degree head- up position with the neck in a
neutral position to improve cerebral venous drainage.
Modest hyperventilation to maintain an arterial PaCO2
TREATMENT
Care of the patient with acute liver failure is directed at
treatment of life- threatening complications and supportive
care until liver function recovers. If hepatic function does
not recover, transplantation will be required.
e immediate care of this patient was used to control
ICP, as this was the most life- threatening complication of
acute liver failure. Subsequent care was directed at prevention of infection and sepsis. Monitoring of liver function
was undertaken to measure the prognosis for recovery of
hepatic function. Once it was recognized that the liver failure was secondary to acetaminophen toxicity, intravenous
N- acetylcysteine (NAC) was administered. She received a
loading dose of 150 mg/ kg over 1 hour followed by 50 mg/
kg over 4 hours and 100 mg/ kg for 16 hours. Toxic doses
of acetaminophen saturate sulfation and glucuronidation
pathways, and acetaminophen is metabolized to N- acetylpara- benzoquinoneimine (NAPQI), which causes hepatocellular necrosis.6 N- acetylcysteine replenishes hepatic
glutathione stores and may reduce NAPQI.7 Over the
subsequent 72 hours, there was no evidence that liver function was improving. Arterial pH was 7.22 and her blood
lactate level was 4.3mmol/ L despite adequate uid resuscitation. She was consequently listed for emergent liver
transplantation.
of 35mmHg should be used to reduce cerebral blood ow
and lessen the risk of cerebral edema, but profound hypocarbia should be avoided, as it may severely decrease cerebral bloodow.
Replacement of coagulation factors is indicated, since
the patient is undergoing an invasive procedure. Factors
V and VII levels are low in patients with acute liver failure
because these two factors have the shortest half- lives (factor V:12– 36 hours; factor VII: 2– 5 hours).4 Factor VII
infusion immediately prior to surgery (40– 80 ug/ kg) may
suce for implantation of an intracranial pressure (ICP)
monitor.5 e severity of the coagulopathy in this patient
(INR > 10), however, warranted administration of fresh
frozen plasma and factor VII. She received 40 ug/ kg of
factor VII and two units of FFP. e repeat INR prior to
FOLLOW- UP
is patient received a liver transplant, and ammonia levels
declined rapidly aer transplantation.8 Survival aer liver
transplantation for acute liver failure has increased substantially over the past 40years, but is still less than survival for
patients undergoing elective transplantation. Although there
are criteria used to gauge the need for acute liver transplantation (Table 36.2), the decision for emergent liver transplantation is controversial and guidelines are not denitive.
9,10
is
patient, however, was not responding to medical therapy and
transplantation seemed to be the only option. Expected survival aer emergent liver transplantation for this young adult
patient with isolated liver failure is60%.
ACUTE LIVER FAILURE 255
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