COLANGITIS
In 1877, Charcot
described cholangitis as a triad of findings of right upper quadrant (RUQ)
pain, fever, and jaundice. The Reynolds pentad adds mental status changes and
sepsis to the triad. A spectrum of cholangitis exists, ranging from mild
symptoms to fulminant overwhelming sepsis. With septic shock the diagnosis
can be missed in up to 25% of patients. Consider cholangitis in any patient who
appears septic, especially in patients who are elderly, jaundiced, or who have
abdominal pain. A history of abdominal pain or symptoms of gallbladder colic
may be a clue to the diagnosis.
·
Charcot's triad
consists of fever, RUQ pain, and jaundice. It is reported in up to 50-70% of
patients with cholangitis. However, recent studies believe it is more likely to
be present in 15-20% of patients.
·
Fever is present in
approximately 90% of cases.
·
Abdominal pain and
jaundice is thought to occur in 70% and 60% of patients, respectively.
·
Patients present with
altered mental status 10-20% of the time and hypotension approximately 30% of
the time. These signs, combined with Charcot's triad, constitute Reynolds
pentad.
·
Consequently, many
patients with ascending cholangitis do not present with the classic signs and
symptoms.
·
Most patients complain
of RUQ pain; however, some patients (ie, elderly persons) are too ill to
localize the source of infection.
·
Other symptoms include
the following:
·
Jaundice
·
Fever, chills, and
rigors
·
Abdominal pain
·
Pruritus
·
Acholic or hypocholic
stools
·
Malaise
·
The patient's medical
history may be helpful. For example, a history of the following increases the
risk of cholangitis:
·
Gallstones, CBD stones
·
Recent cholecystectomy
·
Endoscopic
manipulation or ERCP, cholangiogram
·
History of cholangitis
·
History of HIV or
AIDS: AIDS-related cholangitis is characterized by extrahepatic biliary edema,
ulceration, and obstruction. The etiology is uncertain, but it may be related
to cytomegalovirus or Cryptosporidiuminfections. The management of this condition is described below,
although decompression is usually not necessary.
One of the more common
causes of acute hepatitis is hepatitis A virus (HAV), which was isolated by
Purcell in 1973. Humans appear to be the only reservoir for this virus. Since
the application of accurate serologic investigations in the 1980s, the
epidemiology, clinical manifestations, and natural history of hepatitis A have
become apparent.
The relative frequency
of HAV as a cause of acute hepatitis has declined in Western societies, while
in contrast, notification of individual cases has increased, primarily as a
result of improved reporting and diagnostic techniques. The nadir of reported
cases was in 1987.
Improvements in
hygiene, public health policies, and sanitation have had the greatest impact on
hepatitis A, and vaccination and passive immunization have successfully led to
some reduction in illness in high-risk groups.
Reduced encounters
with HAV at a young age have resulted in both a decline in herd immunity and a
change to the epidemiology of the illness, with increases in the mean age of
occurrence of illness attributed to acute HAV infection in Western societies.
Although this phenomenon may lay a framework for potential epidemics in the
future, public health policies and newly implemented immunization practices are
likely to reduce this potential.
Most patients have no
defined risk factors for hepatitis A. Risk factors for the acquisition of
hepatitis A include the following:
·
Personal contacts
·
Institutionalization
·
Occupation (eg,
daycare)
·
Foreign travel
·
Male homosexuality
·
Illicit parenteral
drug use
HAV is a single-stranded, positive-sense, linear RNA enterovirus
of the Picornaviridae family. In humans, viral replication depends on
hepatocyte uptake and synthesis, and assembly occurs exclusively in liver
cells. Acquisition results almost exclusively from ingestion (eg, fecal-oral
transmission), although isolated cases of parenteral transmission have been
reported.
HAV is an icosahedral nonenveloped virus measuring approximately
28 nm in diameter (see the image below). Its resilience is demonstrated by its
resistance to denaturation by ether, acid (pH 3.0), drying, and temperatures as
high as 56°C and as low as -20°C. The hepatitis A virus can remain viable for
many years. Boiling water is an effective means of destroying it, and chlorine
and iodine are similarly effective.