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Reference Range,
Variable Adults On Presentation 7 Hr after Presentation
Hemoglobin (g/dl) 13.517.5 14.6 12.1
Hematocrit (%) 41.553.0 40.6 34.1
White-cell count (per mm3) 450011,000 8000 10,700
Platelet count (per mm3) 150,000400,000 209,000 148,000
Neutrophils (%) 4070 49
Sodium (mmol/liter) 135145 141 139
Potassium (mmol/liter) 3.44.8 3.8 3.6
Chloride (mmol/liter) 100108 98 101
Carbon dioxide (mmol/liter) 2332 24.3 27.1
Urea nitrogen (mg/dl) 825 17 10
Creatinine (mg/dl) 0.601.50 1.21 1.08
Glucose (mg/dl) 70110 123
Calcium (mg/dl) 8.510.5 10.1 9.2
Albumin (g/dl) 3.35.0 4.9 4.3
Lipase (U/liter) 1360 47 39
Amylase (U/liter) 3100 25 38
Alanine aminotransferase (U/liter) 1055 51 284
Aspartate aminotransferase (U/liter) 1040 42 196
Alkaline phosphatase (U/liter) 45115 72 103
Total bilirubin (mg/dl) 01.0 0.8 5.0
Direct bilirubin (mg/dl) 00.4 0.2 2.6
Troponin I Negative Negative
Troponin T (ng/ml) <0.03 <0.01
* To convert the values for urea nitrogen to millimoles per liter, multiply by 0.357. To convert the values for creatinine to
micromoles per liter, multiply by 88.4. To convert the values for glucose to millimoles per liter, multiply by 0.05551. To
convert the values for calcium to millimoles per liter, multiply by 0.250. To convert the values for bilirubin to micromoles
per liter, multiply by 17.1.
Reference values are affected by many variables, including the patient population and the laboratory methods used. The
ranges used at Massachusetts General Hospital are for adults who are not pregnant and do not have medical conditions
that could affect the results. They may therefore not be appropriate for all patients.
normal. A urine toxicology screen revealed can- Dr. Dudzinski: Aspirin, clopidogrel, intravenous
nabinoids, and a blood toxicology screen was morphine sulfate, lorazepam, ranitidine, alu-
negative; other laboratory test results are shown minum hydroxidediphenhydraminelidocaine
in Table 1. An electrocardiogram showed con- magnesium hydroxide, and intravenous infusions
cave ST-segment elevations (1 to 2 mm) in the of heparin and nitroglycerin were administered,
inferior leads and V3 through V6 precordial leads, and emergency coronary angiography was ar-
along with a PR-segment elevation in lead aVR ranged. A diagnosis was made.
and possible subtle PR-segment depressions
(Fig. 1). Imaging studies were obtained. Differ en t i a l Di agnosis
Dr. Matthew P. Moy: A chest radiograph was
normal. The lungs were clear, and there was Dr. Douglas E. Drachman: This previously healthy
no evidence of pneumothorax, cardiomegaly, or 32-year-old man, who had a history of illicit-
mediastinal widening. drug use and a family history of premature heart
dial oxygen.4 Could this patient have used cocaine asymmetric pulses, bruits, and diastolic murmur)
recently? The urine and blood toxicology screens on clinical examination.6,7 In patients in this
were negative for the presence of cocaine, but in patients age group, connective-tissue disorders
some instances, a toxicology screen yields a nega- might confer a predisposition to aortic dissec-
tive result within a few days after cocaine use. tion, but in this case, there was no evidence in
Factors that argue against a diagnosis of the history or on physical examination to sup-
acute myocardial infarction include the history port the diagnosis of connective-tissue disease.
of pain after eating, the insidious onset and
abrupt worsening of symptoms, and the repro- Acute Vascular Diseases
ducible pain on palpation.3 In addition, the mor- Is this patients presentation consistent with a
phologic features of the ST segments on electro- systemic or mesenteric acute vascular disease?
cardiography did not clearly indicate a current The postprandial onset of severe pain in the
of injury pattern, which is seen in acute myo- subxiphoid area raises concerns about acute
cardial infarction, and a test for troponin I was mesenteric ischemia. Use of cocaine and mari-
negative, although the proximity of testing to juana may provoke an arteriopathy, which could
the onset of symptoms may not have permitted involve the mesenteric arteries. Acute mesenteric
adequate time for the detection of myocardial ischemia, however, more commonly results from
necrosis. a cardioembolic event, such as atrial fibrillation.
The patients recent episodes of emotional There were no findings on examination to sug-
stress may be implicated as a possible inciting gest peripheral embolization. Furthermore, the
factor of a coronary ischemic event. In addition, blood amylase and lipase levels were not elevat-
substantial acute emotional stress may provoke ed, whereas elevated levels might be anticipated
the development of takotsubo (stress) cardiomy- in a patient with acute mesenteric ischemia.
opathy, a syndrome that is classically character- Celiac-artery dissection is rare but can occur
ized by severe left ventricular apical dysfunction, in a young, otherwise healthy man. It often oc-
which may mimic an acute myocardial infarc- curs after an event, such as abdominal trauma,
tion but occurs in the absence of epicardial sneezing or coughing, lifting of heavy objects, or
coronary disease.5 The syndrome is rare in young an abrupt increase in abdominal pressure asso-
men and commonly occurs immediately after ciated with swinging a golf club. The median
a profound, abrupt episode of stress. The ab- arcuate ligament syndrome could also be consid-
sence of an elevated troponin I level also makes ered in this case.8 In this congenital syndrome,
takotsubo cardiomyopathy unlikely. the median arcuate ligament of the diaphragm
crosses over the celiac artery, and this results in
Aortic Dissection extrinsic compression of the vessel and associ-
On rare occasions, a young patient (in this pa- ated mesenteric ischemia. Persons with this con-
tients age group) presents with suspected myo- dition may have insidiously progressive ab-
cardial infarction but has type A aortic dissection. dominal and postprandial pain as the ligament
On examination, this patient had hypertension, encroaches on the entire celiac artery. It would
which could be a reflection of stress or clini- be rare for a patient with the median arcuate
cally significant pain but could also indicate ligament syndrome to present with the abrupt
underlying vascular or aortic disease. In a young, onset and severe pain seen in this patient. Neither
previously healthy man, however, the develop- celiac-artery dissection nor the median arcuate
ment of aortic dissection is more commonly ligament syndrome would result in electrocar-
preceded by a provocation, such as lifting of diographic changes, and therefore these entities
heavy weights, followed by the abrupt onset of are not high in the differential diagnosis for this
severe (tearing) pain in the interscapular, chest, patient.
or abdominal region.6,7 Although clinicians should Systemic vasculitis would confer a predisposi-
be aware of the possibility of aortic dissection, it tion to early adverse cardiovascular events in this
is unlikely that this patient has this diagnosis, patient and could have done so in his father.
given the postprandial onset of symptoms and Fibromuscular dysplasia in the renal arteries
the absence of characteristic findings (e.g., could lead to hypertension in a young patient
and could increase the risk of cardiovascular ischemia is not my leading diagnosis in this case
disease. In a patient with systemic vasculitis, because critical laboratory data were obtained
findings on physical examination might include that will allow us to reframe the initial diagnos-
joint laxity (which is associated with the Ehlers tic considerations.
Danlos syndrome), a bifid uvula and facies (which In learning more about the evolution of this
are associated with the LoeysDietz syndrome), patients hospital course, we have been provided
and classic findings associated with Marfans with additional laboratory data. Seven hours after
syndrome, but in this patient, neither the history presentation, the alanine and aspartate amino-
nor examination yielded additional evidence of transferase levels were four times as high as the
these disorders. levels at presentation and the bilirubin level was
Venous thromboembolic disease also merits more than five times as high as the upper limit
consideration. Pulmonary embolism, which clas- of the normal range. The presence of such liver-
sically mimics myocardial infarction,9 is a consid- function abnormalities in a patient with no signs
eration in this patient who presented with dys- of cardiogenic shock or congestive heart failure
pnea and mild tachypnea and diaphoresis. The points us away from a cardiac diagnosis. Does
location of the pain in the subxiphoid area may the acute rise in aminotransferase levels signify
indicate that the pain was thoracic in origin, but an embolus to the hepatic artery or a dissection
the pain was definitively not pleuritic in nature. of the celiac artery? We do not know the patients
The absence of tachycardia and hypoxemia also ethnic background or red-cell indexes (e.g., mean
makes pulmonary embolism unlikely, although it corpuscular volume), but sickle cell disease can
should be noted that the heart rate of 83 beats per result in arterial occlusion in the liver and as-
minute might be moderately elevated, given the sociated abdominal pain. Could this patient have
patients age and previous health status. the BuddChiari syndrome or a process that
leads to elevated pressures and congestion in the
Noncardiovascular Causes of Chest Pain hepatic veins? It is unlikely that the abrupt onset
Noncardiovascular causes of chest pain may of pain after eating, which was described by this
mimic cardiovascular disease. A gastric ulcer, patient, would be consistent with a diagnosis of
biliary colic, and a Schatzkis ring may each lead the BuddChiari syndrome.
to pain in the subxiphoid area that may occur Acute cholecystitis is a diagnosis that war-
after eating. Some cases of musculoskeletal in- rants careful consideration. At the time of pre-
jury and herpes zoster have resembled acute sentation, this patient had some features that
myocardial infarction, but neither cause seems were typical for cholecystitis, including persis-
likely in this case. tent postprandial pain, increasing bilirubin and
aminotransferase levels, and mild leukocytosis.
Additional Diagnostic Considerations Tenderness in the subxiphoid area could poten-
What types of cardiovascular testing might we tially be consistent with acute cholecystitis, al-
have considered if we had evaluated the patient though the patient did not describe pain in the
at the time of presentation? Transthoracic echo- right upper quadrant. The change in the labora-
cardiography is a noninvasive study that could tory test results over time makes cholecystitis a
help to identify focal left ventricular hypokine- likely cause. Case reports have described patients
sis, which would indicate a territory of ischemia with subdiaphragmatic acute processes who have
associated with a coronary artery, stress cardio- ST-segment elevation on electrocardiography that
myopathy, or a pericardial abnormality or effu- is due to diaphragmatic irritation.10,11 Canine
sion. Computed tomographic angiography could models of acute occlusion of the common bile
help to identify aortic dissection, aortic aneu- duct have revealed sluggish blood flow in the
rysm, mesenteric-artery dissection, or embolus coronary arteries, which is possibly due to
to a visceral artery and could possibly help to changes in coronary microvascular tone; such
rule out pulmonary embolism. In this patient, changes could also explain the abnormal elec-
coronary angiography may have been performed, trocardiographic findings seen in this case.12
since it is the standard study for the diagnosis My recommendation for establishing the di-
of coronary-artery stenosis. However, coronary agnosis would be to perform ultrasonography
Cl inic a l Di agnose s
Biliary pain due to cholecystitis or choledocholi-
thiasis.
no evidence of a mass or bleeding. Biliary sphinc- per quadrant, and he had some tenderness in the
terotomy was performed. right upper quadrant on examination.
Although ultrasonography has high sensitivity When we considered the possibility that this
and specificity for the detection of acute chole- patient had choledocholithiasis, we were dis-
cystitis, false negative examinations can occur. suaded by the absence of dilatation of the com-
The cause of acute calculous cholecystitis is mon bile duct on ultrasonography and the ab-
considered to be obstruction of the cystic duct, sence of ductal filling defects on ERCP. However,
and it is notable that the cystic duct was patent we thought that a gallstone could have caused the
on ERCP in this patient. It is possible that the underlying problem and then passed through the
retrograde injection of contrast material under common bile duct into the duodenum, which
pressure during ERCP could cause opacification would explain why there was no evidence of cho-
of the cystic duct. There were no findings on the ledocholithiasis on ultrasonography and ERCP. In
imaging studies to suggest biliary obstruction or light of this possibility, we elected to perform lapa-
choledocholithiasis; however, if the patient had roscopic removal of the gallbladder, not to treat the
spontaneously passed a stone, the results on acute condition but to prevent a future similar pre-
abdominal ultrasonography and ERCP may have sentation with obstruction of the common bile duct.
appeared to be normal. We approached the operation with the inten-
Dr. Dudzinski: Dr. Fernandez-del Castillo, tion of performing a semielective cholecystecto-
what was your clinical impression and initial my. However, during the procedure, we found a
treatment strategy when you evaluated this pa- very distended gallbladder with a gangrenous
tient? wall that had adhered to the omentum. On the
basis of the findings on ultrasonography, we
had not expected to find a thickened gallbladder
Surgic a l A sse ssmen t
a nd M a nagemen t wall. The gallbladder was so distended and full
that we could not grasp it initially and had to
Dr. Carlos Fernandez-del Castillo: This patient present- empty it before removal. The surgical dissection
ed with nearly normal results on liver-function was laborious and required placement of a surgi-
tests, and within 1 day, his bilirubin level reached cal drain, which we normally would not do after
5 mg per deciliter (85.5 mol per liter). Our ini- a laparoscopic cholecystectomy.
tial differential diagnosis included acute chole-
cystitis and choledocholithiasis. Simultaneous Pathol o gic a l Discussion
acute cholecystitis and choledocholithiasis would
be rare, because the cause of acute cholecystitis Dr. Jonathan H. Chen: The cholecystectomy speci-
is obstruction of the cystic duct whereas the cause men was tannish pink and had focal areas of
of choledocholithiasis is obstruction of the com- hyperemia and hemorrhage. The opened gall-
mon bile duct. Patients with acute cholecystitis bladder had small amounts of greenish brown
may have jaundice and an elevated bilirubin level, bile and yellowish brown biliary sludge, along
but the bilirubin level rarely rises above 4 mg per with a large number of irregular, roughly spher-
deciliter (68.4 mol per liter). Features of this ical yellow and yellowish green calculi, which
patients presentation that argue against a diag- ranged from 2 to 15 mm in greatest dimension.
nosis of acute cholecystitis include the absence The gallbladder wall measured up to 4 mm in
of fever, emesis, and any other gastrointestinal thickness (normal thickness, <3 mm). Micro-
symptoms. In addition, he did not have clinical- scopic examination revealed a lymphocytic and
ly significant leukocytosis or have gallbladder- neutrophilic infiltrate that extended transmu-
wall thickening or Murphys sign on ultrasonog- rally from the mucosa to the serosal and adven-
raphy; these findings are all characteristic of titial surfaces (Fig. 3). The gallbladder wall was
acute cholecystitis. However, the pain shifted fibrotic and hemorrhagic and had surface necro-
from the center of his abdomen to the right up- sis. There was no evidence of cancer.
past infection and in defining the cause of cho- A nat omic a l Di agnosis
lesterol-stone formation.
Dr. Dudzinski: The patient had an uneventful Acute and chronic cholecystitis and extensive
course after the cholecystectomy. The surgical cholelithiasis with transmural gallbladder in-
drain was removed before discharge, on post- flammation.
operative day 2. He completed a 10-day course This case was presented at the Medical Case Conference.
of ciprofloxacin and clindamycin. Three weeks Disclosure forms provided by the authors are available with
the full text of this article at NEJM.org.
later, he presented for a postoperative follow-up We thank Dr. Gaurav A. Upadhyay for contributions to the
visit and was well. case history.
References
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EM, et al. The International Registry of ischemic ECG changes in a patient with Copyright 2017 Massachusetts Medical Society.
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