Chief Complaint: epigastric pain
History of Present Illness:
Eleven years PTA (1997), the patient has had an acute cholecystitis and had undergone cholecystectomy. Before the operation, she presented with epigastric pain with a severity of 10/10 that radiated to the right interscapular region. Jaundice with acholic stools and tea-colored urine were noted. Patient was afebrile then. Post-operation, she became asymptomatic and was advised by the physician to refrain from eating fatty meals, softdrinks, etc.
Two weeks PTA, the patient has experienced epigastric pain in four consecutive days. The pain is poorly localized and was graded 8/10 and seemed to radiate to the right interscapular region. Each episode occurred 3 hours after lunch that prompted her to consult in a hospital in Talavera, Nueva Ecija where she was injected with Tramadol (and/or Buscopan – unrecalled by patient) and Ranitidine. These gave her relief after 1½ hours however, she developed an allergic reaction to Ranitidine; this manifested as erythematous macules on the extremities, on the dorsal trunk, on the neck and on the waistline area. On the fourth day (fourth episode), she also presented with jaundice which caused her admission to the hospital (
Past History:
Medical:
Patient has no childhood illnesses. At age 35, she was known to have asthma which is managed with Ventolin taken prn. Last attack was 1½ weeks ago.
Surgical:
Patient has undergone open cholecystectomy (1997) indicated for acute cholecystitis secondary to gallstones; she was transfused with 2 units of blood during the operation.
Obstetric/Gynecological:
Menarche-age: 16 y/o
Menopausal-age: N/A
Menstrual flow-interval: 28-30 days (however, menstruation stops for 4 months)
Duration: 3 days
Amount: 2 pads/day
LMP: March 28-
Obstetrical History: G3P3 (3003).
Family History:
Aunt and Uncle have asthma. No other diseases among the family members.
Personal and Social History:
Patient is a plain housewife. She has a good relationship with her family and relatives.
Her diet consists of mixed diet. She is a non-smoker and non-alcoholic drinker; she denies illicit drug use.
Review of Systems:
General: (+) Weight loss (loose clothing from onset of abdominal pain to post-op)
(+) weakness, (-) fever, chills
Skin: (+) pruritus, (+) icteric skin, (+) rash
HEENT: (+) icteric sclera, (-) visual problems, hearing difficulties, epistaxis, discharge, bleeding gums, tonsillitis
Neck: unremarkable
Breast: unremarkable
Pulmonary: unremarkable
Cardiac: unremarkable
Vascular: unremarkable
GI: refer to HPI
GU: unremarkable
Musculo-S: unremarkable
Endocrine: unremarkable
Hemapoietic: unremarkable
Neurologic: unremarkable
Psychiatric unremarkable
Physical Examination: [June 18, 2008/1:30PM]
Wt: 50kg Ht: 162cm BMI: 19.5
BP: 115/80 Temp: 36.5ºC PR: 72/min, reg RR: 19/min, reg
Patient was conscious, coherent, ambulatory and not in cardiorespiratory arrest. She smiled occasionally, with appropriate mood and affect. Voice was audible, alert. General weakness/fatigue is noted (due to lack of sleep and water/juice diet after ERCP on June 17).
She presented with warm moist skin, some itching, scratch wounds on the extremities especially the dorsal trunk, violet/dark faded macules on the extremities and trunk; no yellowish discoloration of the skin. She had pink palpebral conjunctiva, icteric sclera; no nasal and auditory discharge; mosit buccal mucosa with icteric frenulum. The neck was supple; there were no neck vein distention, no palpable cervical lymph node, and no thyroid gland enlargement. She had clear breath sounds, adynamic precordium, apical beat was felt at the 5th LICS MCL; S1>S2 at the apex and S2>S1 at the base; there were no murmurs, heaves, lifts or thrills. Her abdomen was flat and symmetrical with silver striae, scratch wounds/abrasions on the waistline area and two scars from previous operation: one is circular, measuring 1 x 1 cm in diameter located 10 o’clock of the umbilicus, the other is a 4-inch oblique linear scar 3 inches inferior to the right subcostal margin; umbilicus is midline and everted; on auscultation 16 peristaltic waves per minute was noted, there were no bruits or friction rubs; on percussion all quadrants were tympanitic; on palpation abdomen was soft, there was no tenderness on light palpation, deep palpation was not done because patient was post-op, no fluid waves; no hepatosplenomegaly (liver span is 8.5cm R MCL).
No cyanosis, bipedal edema, or clubbing were appreciated. Her pulses were full and equal. Neurologic exam was unremarkable.
D I S C U S S I O N
Note: The interview was done post-op. Discussant will focus on the patient’s history.
Salient Features
Subjective:
Epigastric pain
grade 8/10
radiation to the right interscapular area
usually occurred 3 hours after lunch
relieved by pain relievers, antispasmodic
associated manifestations:
jaundice
pruritus
acholic stools
dark urine (tea-colored)
Objective:
52 years old
Female
Jaundice
Cholecystitis s/p cholecystectomy (1997)
(-) hepatomegaly
Assessment
Biliary obstruction secondary to recurrent cholelithiasis s/p cholecystectomy (1997)
Obstruction in the biliary tree manifests with abdominal pain that is of biliary colic type, meaning the pain is steady lasting at least 30 minutes and up to several hours. Patients may also feel right upper quadrant pain, others manifest with right flank pain. Radiation to the back and shoulders is not uncommon. The onset of pain is a few hous after meals and may wake patient at night. Associated manifestations are jaundice and pruritus. Most of the said clinical presentations were appreciated in the patient.
Biliary obstruction due to a recurrent stone is very likely in this case because of the following predisposing factors: patient is a female, is above 40 years old, has a history of cholelithiasis and had undergone cholecystectomy. These (and the more definitive objective finding of gallstones in her ultrasound) point out to the assessment.
Differential diagnoses
The basis of the differentials is the epigastric pain along with jaundice. If patient has not revealed the result of the ultrasound, the following are being considered for this case.
Intrahepatic causes:
Hepatitis
Primary Biliary Cirrhosis
Primary Sclerosing Cholangitis
Extrahepatic causes:
Cholangiocarcinoma
Pancreatic Cancer
Ampullary Cancer
Primary Sclerosing Cholangitis
Chronic Pancreatitis
Biliary Duct Stricture
Long Cystic Duct Stump
Sphincter of Oddi Dysfunction
Hepatitis is among the differentials because of the presentation of jaundice, pruritus (and rashes), epigastric pain, acholic and dark urine. In addition, the patient has a history of blood transfusion (1997) which may have been the route of this inflammatory disease. However the patient does not present with hepatomegaly or liver tenderness, she was afebrile, and she did not experience arthralgias or myalgias.
For same reasons as the symptom presentation in hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis are considered but then again, liver and spleen was not palpable in the patient. Moreover, the patient did not report of fatigue which is the most prevalent feature of primary biliary cirrhosis. No febrile episodes were noted which is common in cholangitis.
Cholangiocarcinoma, pancreatic cancer, and ampullary cancer may be included in the differentials because they present with same symptoms (jaundice, epigastric pain). In support to carcinomas, the patient noted weight loss. However, there were no palpable mass/es.
Chronic pancreatitis is also possible in this patient since there is history of cholelithiasis which is among the top causes of pancreatitis.
The above mentioned differentials will all lead to biliary duct strictures which is the ultimate reason for symptoms to manifest. These strictures may be benign or malignant. The benign ones are a result of injury to the bile ducts—from surgery (the patient have undergone cholecystectomy in 1997) or trauma or from recurring or chronic conditions like pancreatitis, cholelithiasis, cholecystitis, primary sclerosing cholangitis, among others. The injury produces an inflammatory response followed by collagen deposition, fibrosis and narrowing of the bile duct caliber. This may progress to high grade strictures after they atrophy (damaged parts) then hypertrophy (uninjured parts) which result to biliary cirrosis and portal hypertension. The malignant strictures on the other hand, result from a primary bile cancer that obstructs bile flow (e.g. cholangiocarcinoma) or extrinsic compression of the bile from a neoplasm of the adjacent organs (pancreatic cancer or ampullary cancer).
A post-cholecystectomy condition termed sphincter of oddi dysfunction (SOD) is suggested in this case. This is suspected in patients with typical episodic biliary-type of pain without an obvious organic cause. Approximately 1% of patients who underwent cholecystectomy are estimated to have SOD.
Pathophysiology, Pathogenesis, Discussion
The prominent features in the case are epigastric pain which was characterized as continuous and dull, graded 8/10, occurring 3 hours after meals, radiating to the right interscapular area, relieved by pain relievers and antispasmodic. Jaundice, pruritus, acholic stools and tea-colored urine are the associated manifestations.
It is important to note that the patient is a 52 year old female who had undergone cholecystectomy in 1997 due to acute calculous cholecystitis. The physical examination revealed no hepatosplenomegaly.
Basing on these, patient is assessed to have biliary obstruction secondary to recurrent cholelithiais s/p cholecystectomy (1997).
The patient is prone to develop recurring gallstone disease because of her gender, age and history of cholelithiasis (other predisposing factors are ethinic background, obesity, pregnancy and diet). Females are three time more likely to develop gallstones (Beauchamp et.al., 2004). Estrogen stimulates hepatic lipoprotein receptors, increase uptake of dietary cholesterol, and increase biliary cholesterol secretion. Age is another factor since increasing age means increased biliary secretion of cholesterol, decreased size of bile acid pool and decreased secretion of bile salts (Kasper, et.al., 2005). Post-cholecystectomy, patients have 20% chance of experiencing abdominal pain months to years following the procedure (Beauchamp et.al., 2004). In this case, a recurrent stone rather than retained stone is probable. Retained stone occurs within two years of cholecystectomy while recurrent stones are those detected more than two years after operation.
Gallstones are formed by concretion or accretion of normal or abnormal bile constituents. They are divided into two major types: cholesterol stones (80%) and pigment stones (~20%). The pathogenesis of cholesterol stones are influenced by four conditions: 1) bile must be supersaturated with cholesterol, 2) gallbladder hypomotility promotes crystal nucleation, 3) cholesterol nucleation in bile is accelerated, and 4) mucus hypersecretion in the gallbladder traps the crystals, permitting their agglomeration into stones. Nucleation is promoted by microprecipitates of calcium salts (inorganic or bilirubin salts). The pathogenesis of pigment stones on the other hand, is based on the presence in the biliary tree of unconjugated bilirubin and precipitation of calcium bilirubin salts (Robbins et.al., 1999). The most important mechanism in the development of lithogenic bile is increased biliary secretion of cholesterol in relation to phospholipids and bile acids.
Biliary obstruction is caused primarily (90% of the time) by these gallstones. This presents with biliary colic pain and jaundice. The biliary colic type of pain is caused by the sudden distention of the biliary tree due to obstruction (usually in the common bile duct). This obstruction leads to bile accumulation in the liver, i.e. there is impaired uptake, conjugation or excretion of bilirubin which causes the jaundice (icteric sclerae, skin and frenulum).
Plans
Diagnostic:
Serum ALT, AST
Alkaline phosphatase
CBC
Prothrombin Time
Albumin
Hepatobiliary ultrasound
Endoscopic retrograde cholangiopancreatogram (ERCP)
Percutaneous transhepatic cholangiogram (PTC)
Management:
Endoscopic retrograde cholangiography (ERCP)
In cholestatic conditions that cause jaundice, the plan is to determine if it is intra- or extrahepatic cholestasis. The laboratory tests will help facilitate diagnosis and rule out other diseases.
Serum ALT and AST in patients with cholestasis is usually only moderately elevated but occasionally may be markedly increased, especially if cholangitis is present. In extrahepatic cholestasis, usually, serum AST levels are not elevated unless secondary acute parenchymal damage is present while in intrahepatic cholestasis, ALT and AST are elevated, with predominace of ALT. Alkaline phosphatase is markedly elevated in persons with biliary obstruction. However, high levels of this enzyme are not specific to cholestasis. In extrahepatic obstruction, ALP levels are elevated in nearly all patients, except in some cases of incomplete or intermittent obstruction. Values are usually greater than 3 times the upper limit of the reference range, and in most typical cases, they exceed 5 times the upper limit. An elevation less than 3 times the upper limit is evidence against complete extrahepatic obstruction. PT may be prolonged due to malabsorption of vitamin K. Correction of the PT by parenteral administration of vitamin K may help distinguish hepatocellular failure from cholestasis. Little or no improvement occurs in patients with parenchymal liver disease.
The history, physical examination and the laboratory examinations only provide clues so that the next appropriate approach is a hepatobiliary ultrasound. This is inexpensive and radiation-free; detects intra- and extrahepatic biliray tree dilation with high degree of sensitivity and specificity. The absence of biliary dilation will point a intrahepatic cholestasis while presence of biliary dilation indicates extrahepatic cholestasis. However, ultrasound may not indicate site of obstruction because the common bile duct is difficult to visualize, hence either a CT scan or ERCP is the next step. In this case, ERCP is preferred. ERCP is the gold standard for identifying choledocholithiasis. It is performed by introducing a side-viewing encoscope perorally into the duodenum and allows visualization of the ampulla of vater, common bile duct and pancreatic duct. It is also a therapeutic intervention which is why this is opted. If common bile duct stones are seen, this procedure allows removal or extraction of common bile duct stones. Moreover, if need be, stents may be placed, bile or pancreatic cytology, endoscopic sphincterotomy and biliary manometry may be perfomed via ERCP. PTC may be performed if ERCP is unsuccessful. This provides same information as ERCP. If there is suspicion of intrahepatic cholestasis, serologic testing plus percutaneous liver biopsy is indicated.
