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17 Critical Care Management of Severe Acute Pancreatitis
203
Patients with clinical evidence of acute hemorrhage who
are stable or who have sequelae of recent (peri)pancreatic
hemorrhage on CT should undergo CTA to evaluate for the
development of pseudoaneurysms. Patients with acute hemorrhage who have hemodynamic compromise that improves
with resuscitation and patients with negative CTA with signs
of peripancreatic hemorrhage should undergo angiography.
Most pseudonaeurysms can be interventionally treated with
embolization or covered stent isolation with improved morbidity and mortality compared to open surgical techniques.
Patients with hemodynamic compromise secondary to pancreatic hemorrhage who do not respond to resuscitation may
require acute surgical intervention. The use of REBOA in
these patients may be lifesaving as a bridge to surgical or
interventional therapy.
Summary
Pancreatitis is the most common gastrointestinal disease process requiring hospital admission and severe cases continue
to have a high morbidity, mortality, and cost of care. The
initial aspect of management is predicting which patients
with acute pancreatitis will go on to develop severe forms of
the disease. Unfortunately, most of the severity indices and
classifi cation systems used to assist in this process are either
imprecise or require several days to complete, at which point
severe disease is apparent. There are however a number of
features that can be evaluated at presentation (Table 17.5 )
and can be helpful in identifying those at risk for severe disease. The subsequent ICU management of severe acute pancreatitis can be divided into phases that correspond with the
pathophysiologic stages of severe disease.
Care in the fi rst 24 h is focused on prevention of the development of pancreatic necrosis and persistent organ failure
and mitigation of the overall disease process. Carefully
guided resuscitation, avoidance of over-resuscitation, monitoring for and treatment of the development of intraabdominal hypertension and abdominal compartment
syndrome, and acute support for organ failure are the key
features.
The fi rst week of treatment is characterized by support for
organ failure, continued monitoring of IAH, and specifi c
therapies to minimize the risk of the development of local
complications. The only therapy that has been shown to minimize the development of infected pancreatic necrosis,
decrease local complications, and improve outcomes and
mortality is early enteral nutritional therapy, which should be
started within the fi rst 48 h. There is currently no role for
prophylactic antibiotics or probiotics to prevent the development of infected pancreatic necrosis. Routine endoscopic
therapy in the fi rst few days does not change the acute phase
of the disease process or improve outcomes, except for
patients presenting with ampullary obstruction or cholangitis. However, after the initial acute phase, ERCP and ES
should be considered to prevent recurrence for patients with
biliary causes of pancreatitis in whom early cholecystectomy
is not possible. Patient with severe acute pancreatitis should
be investigated for elevated triglycerides within the fi rst
2 days, and therapy should be instituted when they are
>1,000 mg/dl.
The subsequent weeks of ICU care are characterized by
ongoing nutritional support, treatment for persistent organ
dysfunction, and vigilant monitoring for the development of
local complications and infection. Patients who fail to improve
or have an acute decline in their status should be carefully
investigated for their development. Modern minimally invasive techniques of percutaneous drainage, angiography,
VARD, and endoscopic therapy have improved morbidity and
mortality and supplanted open surgical management in most
cases. Open surgical treatment still plays a role for the treatment of abdominal compartment syndrome nonresponsive to
medical management; pancreatic necrosis with severe clinical
deterioration in the fi rst week of the disease; infected pancreatic necrosis not amenable or responding to minimally invasive therapy; colonic necrosis, perforation, or stricture; and
acute hemorrhage with hemodynamic compromise.
Though morbidity and mortality remain high in patients
with severe acute pancreatitis, it is likely that an organized,
protocolized approach to their management can improve
outcomes.
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Hepatic Failure
Mario Rueda and Pamela A. Lipsett
1 8
Acute Liver Failure
D e fi nition, Epidemiology, and Causes
Acute liver failure (ALF) refers to the rapid deterioration of
liver function that is seen in previously healthy patients. Its
defi ning characteristics include the development of coagulopathy, with an international normalized ratio (INR) >1.5,
as well as alteration of mental status (encephalopathy). It
occurs in individuals without preexisting cirrhosis and with
an illness of no more than 26 weeks duration.
There are some minor differences that are associated with
duration of symptoms, and therefore ALF can be further subdivided into hyperacute (less than 7 days), acute (7–21 days),
or subacute (more than 21 days and less than 26 weeks).
Hyperacute and acute liver failures are more commonly
associated with cerebral edema, while patients with subacute
failure can present with ascites, portal hypertension-related
bleeding, and renal failure.
Approximately 2,300 patients experience ALF in the
United States [ 1 ]. Half of these cases are associated with drug
toxicity, most of them related to acetaminophen. Viral hepatitis accounts for one fi fth of the cases, the remaining being
different metabolic and vascular disorders (Table
18.1 ) [ 2 ].
Clinical Manifestations
The rapid compromise of hepatic physiologic function
results in clinical features that can affect several organ systems and can be variable in their presence and intensity.
M. Rueda , MD (*) • P. A. Lipsett , MD, MHPE
Department of Surgery , Johns Hopkins Hospital ,
600 N Wolfe Street, Osler 603 , Baltimore , MD 21287 , USA
mrueda3@jhmi.edu; plipsett@jhmi.edu
e-mail:
Neurologic System
Nonspecifi c complaints such as fatigue, malaise, lethargy,
nausea, vomiting, headache, and anorexia are frequently
present in patients with liver failure. As a defi ning characteristic, patients with ALF present with various degrees of
encephalopathy, ranging from slight confusion to coma. In
order to characterize the severity of the impairment, several
grading scales have been described [ 3 ]. Most commonly
used is the West-Haven criteria (Table 18.2 ) [ 4 ]. For moder-
ate to severe cases of encephalopathy, the Glasgow Coma
Scale can also be used.
The mechanism by which these changes occur has not
been fully identifi ed; however, there are some generally
Table 18.1 Causes of acute liver failure
Medications Acetaminophen (paracetamol)
Tetracycline
Troglitazone
Isoniazid
Aspirin
Toxins
Infectious Hepatitis A
Metabolic Acute fatty liver of pregnancy
Vascular Budd-Chiari syndrome
Parenchyma replacement or loss Breast cancer
Amanita mushrooms
Lepiota helveola
Hepatitis B
Hepatitis C (very uncommon)
Cytomegalovirus
Epstein-Barr virus
Wilson’s disease
Reye’s syndrome
Portal vein thrombosis
Veno-occlusive disease
Ischemic hepatitis
Melanoma
Small cell lung cancer
Hepatectomy
Necrosis
© Springer International Publishing Switzerland 2016
N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_18
211
212
M. Rueda and P.A. Lipsett
Table 18.2 West-Haven criteria for grading hepatic encephalopathy
Grade I Trivial lack of awareness
Euphoria or anxiety
Shortened attention span
Impaired performance of addition
Grade II Lethargy or apathy
Minimal disorientation for time or place
Subtle personality change
Inappropriate behavior
Impaired performance of subtraction
Grade III Somnolence to semistupor but responsive to verbal
stimuli
Confusion
Gross disorientation
Grade IV Coma (unresponsive to verbal or noxious stimuli)
accepted theories that revolve around impaired detoxifi cation of substances normally cleared by the liver.
• Ammonia
• The metabolism of nitrogen-containing compounds in the
gastrointestinal system results in the production of ammo-
nia. In its normal state, the liver converts this neurotoxic
product into glutamine and urea. Impaired liver function
results in elevated blood ammonia. Astrocytes contain the
enzyme glutamine synthetase in their endoplasmic reticu-
lum as a means of handling excessive ammonia.
Accumulation of glutamine within the astrocytes results
in cell swelling which leads to a series of events that result
in a neuroinhibitory state [
5 ].
• False Neurotransmitters
• The failing liver results in the production of false neu-
rotransmitters. These molecules may interfere with nor-
mal brain functioning and have a net inhibitory effect [ 6 ].
• Amino Acid Imbalance
• Patients with hepatic failure have decreased plasma levels
of the branched-chain amino acids (BCAA) valine, leu-
cine, and isoleucine while experiencing increased levels of
aromatic amino acids (AAA) phenylalanine, tryptophan,
and tyrosine. This is thought to be related to increased
muscle catabolism and therefore increased BCAA metab-
olism as well as decreased breakdown of AAA by the
compromised liver. The end result is an imbalance that
leads to an increased infl ux of AAA in the brain which has
an inhibitory effect in the nervous system [ 7 ].
• GABA receptor
• Thought to be mediated by infl ammatory cells, neuros-
teroids are produced by myelinated glial cells. This results
in positive modulation of GABA receptors that in turn
enhance the inhibitory tone [
8 ].
Besides the astrocyte swelling that is seen with the accumulation of glutamine explained above, overall neurologic
Table 18.3 Respiratory complications seen in acute liver failure
Infectious Upper respiratory infections
Pneumonia
Noninfectious Pulmonary edema
Pleural effusion
Pneumothorax
Hepatopulmonary syndrome
Acute respiratory distress syndrome
Acute lung injury
Depressed central respiratory drive
dysfunction results in loss of autoregulation of intracranial
pressure as well as reduced cerebral blood fl ow. The result of
these changes may result in further neurologic derangement
and compromise [
9 ].
Besides hepatic encephalopathy, patients with ALF can
also present with cerebral edema. There is an overlap with
the clinical features that are seen with encephalopathy and
include nausea, vomiting, headache, and agitation. In
advanced cases which can progress to brain herniation,
hypertension, bradycardia, changes in pupillary exam or
refl exes, as well as respiratory depression can be seen [ 10 ].
Respiratory System
Patients with ALF may present with nonspecifi c respiratory
symptoms including dyspnea on exertion, orthopnea, anxiety, and air hunger. The affecting processes involved are very
broad and can range from a simple pleural effusion to acute
respiratory distress syndrome (ARDS) [ 11 ]. The spectrum of
respiratory pathology that is seen can be grouped in to two
major categories: infectious and noninfectious (Table 18.3 ).
Pulmonary edema can be of cardiogenic or noncardiogenic etiology. The prevalence of pulmonary edema appears
to be higher in those patients with cerebral edema, suggesting the accumulation of osmotic substances within the lung
parenchyma and outside the vasculature [ 12 ]. Molecular
imbalance and injury to endothelial cells, accompanied by a
decrease in oncotic pressure, may play a role in the development of this disease.
Hepatopulmonary syndrome can be seen in both ALF and
chronic liver failure. It is thought to arise from microscopic
shunting from arteriovenous dilations that occur in the pulmonary vasculature [ 13 ]. The precise mechanism is unknown;
however, it is thought that the elevated levels of nitric oxide
seen in patients with liver failure may mediate the abnormal
vasodilation that occurs in the pulmonary parenchyma. The
result is an overperfusion with maintenance of ventilation; a
VQ mismatch occurs that ultimately leads to hypoxemia [ 14 ].
Cardiovascular and Hematologic System
As part of the pathophysiology associated with ALF, there is
low systemic vascular resistance and a hyperdynamic