(Circulation. 1995;92:3139-3143.)
© 1995 American Heart Association, Inc.
Articles |
Multiorgan Failure After Cardiac Arrest in a 20-Year-Old Man
From the Section of Cardiology, Denver General Hospital, and the Departments of Medicine and of Pathology and Laboratory Medicine, University of Colorado Health Sciences Center, Denver.
Correspondence to Edward P. Havranek, MD, Denver General Hospital, Division of Cardiology 0960, 777 Bannock St, Denver, CO 80204.
Key Words: Clinicopathological Conferences • heart arrest
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Case Presentation |
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 Top Case Presentation  Clinical Discussion Pathological Discussion Final Diagnosis References |
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Brian Dwinnell, MD
A 20-year-old man was admitted to the hospital with acute hepatic failure following a cardiac arrest. He had been well until 2 months before admission, when he began to notice fatigue, myalgias, and easy fatigability. Three weeks before admission, he began to notice malaise, nonproductive cough, and progressive dyspnea. Five days before admission he noticed hemoptysis, and 4 days before admission he was started on erythromycin. He was admitted to another hospital the following day. During that admission, a chest radiograph (Fig 1
) demonstrated a right
lower-lobe infiltrate and cardiomegaly. The AST was 1782, the LDH 2561,
and the INR 1.8. Erythromycin was continued, and ceftazidime was added.
Because of the hemoptysis, he underwent bronchoscopy. The procedure was
complicated by a cardiac arrest. He was intubated and mechanically
ventilated. The following day, the AST was 12 810, the LDH 13 440,
and the INR 8.5. He was transferred to the University of Colorado
Health Sciences Center.
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He was a Native American and lived in southwestern Colorado. He smoked one pack of cigarettes per day. He was a binge user of alcohol and had "sniffed glue" in the past. He denied the use of intravenous drugs. He was on no medications before the initiation of erythromycin. Medications at the time of transfer were dopamine, dobutamine, mannitol, ceftazidime, and erythromycin.
On physical examination, the patient was intubated and did not respond to verbal commands. The blood pressure was 106/57 mm Hg, the pulse was 140 beats per minute, and the temperature was 38.0°C. The respiratory rate was 14 breaths per minute, the same as the set rate of the ventilator. The sclerae were icteric. Rales were heard at the bases of both lungs. On precordial examination, the rhythm was regular, and a third heart sound was present. The liver was not enlarged, and a spleen tip was not palpable. The patient intermittently and spontaneously opened his eyes, but there was no movement of the extremities.
Abnormal laboratory data on admission are given in Table
1. The ECG showed only sinus tachycardia and
low limb lead voltage.
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Shortly after admission to the intensive care unit, the patient developed ventricular fibrillation and was resuscitated. He underwent pulmonary artery catheterization. The pulmonary artery pressure was 60/45 mm Hg, and the mean pulmonary capillary wedge pressure was 40 mm Hg. The cardiac index was 1.8 L · min-1 · m-2. An echocardiogram was of poor quality and demonstrated profound global left ventricular hypokinesis; a Doppler examination was not performed. Intra-aortic balloon counterpulsation was initiated.
Over the next several days, the patient experienced progressive renal failure, and hemodialysis was begun. Serological studies for hepatitis B surface antigen, hepatitis A IgM, and hepatitis C IgM all were negative. Results of thyroid function studies were deemed consistent with a "euthyroid sick" state. An ultrasound examination of the right upper quadrant did not demonstrate dilated biliary ducts. A transjugular liver biopsy revealed centrilobular congestion, early fibrosis, and some periportal polymorphonuclear leukocytes. There were no significant antibody titers to coxsackievirus or echovirus.
On the 17th hospital day, the patient's blood pressure declined steadily. After consultation with the patient's family, further attempts at aggressive support were discontinued, and the patient died. An autopsy was performed.
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Clinical Discussion |
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TopCase Presentation Clinical Discussion Pathological Discussion Final Diagnosis References |
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Edward P. Havranek, MD
This 20-year-old man experienced a rapidly progressive illness with severe dysfunction of liver, kidney, and heart, and involvement of the lung. He died presumably of cardiac failure less than 3 weeks after first coming to medical attention. This patient's situation represents a difficult diagnostic problem with a very tragic outcome; when we have an outcome like this, we all have a responsibility to learn from it.
In a case with multi–organ system involvement, I think it important to take a rigid approach to arriving at a diagnosis. The first step is to go through each bit of information, pulling out everything that is abnormal and putting it on a list. This is analogous to the way one might solve a jigsaw puzzle, first laying all the pieces face up on the table in front of you. Clues from the overall course of the illness and demographic clues are less useful but still may be important.
Nothing on the problem list is pathognomonic for any disease, ie, has 100% specificity. Therefore, I pared the list down by choosing the abnormalities I thought had the highest specificity and organized these abnormalities into syndromes. I think the most logical way to group these findings is as dilated cardiomyopathy, acute hepatocellular necrosis, acute renal failure due to ATN, and hyponatremia/hypokalemia; I will discuss the electrolyte constellation in more detail later.
The next step is to identify a single unifying syndrome. I think the most logical way to unify these syndromes is to say that this patient had a dilated cardiomyopathy, with shock that caused acute hepatic cellular necrosis, acute renal failure, and acute adrenal insufficiency.
Several series in the literature describe patients who had cardiogenic shock from a variety of causes and liver function abnormalities very similar to those in our patient. Birgens et al1 described five patients, four of whom had cardiogenic shock from myocardial infarction; the other had presumed myocarditis. All had markedly elevated transaminases 20 to 100 times the upper limit of normal. Biopsy showed central lobular necrosis with hemorrhage in all five of these patients. Logan et al2 reported on three patients with severe congestive heart failure due to aortic stenosis and with elevations of serum transaminases more than 25 times the upper limit of normal; in two of the patients, there was no apparent cause for the elevation in enzymes other than the heart failure.
Similarly, the clinical situation described for the patient under consideration is clearly associated with ATN. Rasmussen and Ibels3 reported on 143 patients with ATN. In most cases, they implicated several insults; the most common was blood pressure <100 mm Hg. When they looked at patients who had only a single insult associated with ATN, hypotension was most common.
Finally, acute adrenal insufficiency is an interesting potential diagnosis in this patient, explaining the constellation of hyponatremia and hyperkalemia. The pathology is typically bilateral adrenal cortex hemorrhage.4 There are two major predisposing factors4 5 6 for adrenal hemorrhage. One factor is hypercortisolism due to ongoing stress. This patient obviously had sufficient ongoing stress. The second factor is the presence of coagulopathy, which, again, this patient had. The clinical features of acute adrenal insufficiency are highly variable. Patients may present with the signs and symptoms that we associate with chronic adrenal insufficiency, or Addison's disease, such as hyponatremia, hyperkalemia, metabolic acidosis, hypotension, weakness or fatigue, or with unexplained abdominal pain or frank retroperitoneal hemorrhage. In the series reported by Xarli et al,4 64% of patients had congestive heart failure. In their review of 153 patients reported in the literature previously, one third of the patients had heart failure. Because of the strong presence of predisposing factors, the combination of hyponatremia and hyperkalemia, and the ongoing shock, I postulate that this patient had acute adrenal insufficiency due to bilateral adrenal hemorrhage, in turn caused by the combination of coagulopathy and heart failure with shock.
I would now like to focus on finding a specific cause for the
cardiomyopathy. We need to explain a rapidly
progressive syndrome, and for that reason I shall narrow that focus to
the causes of myocarditis. I think it is most helpful to group these
into noninfectious and infectious causes (Table 2).
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With respect to the noninfectious causes, drug hypersensitivities are relatively simple to exclude because before his illness, the patient was not taking any drugs that have been associated with myocarditis.7 I do not believe that substance abuse explains the illness. There are case reports of cardiac disease associated with chronic ongoing use of inhaled hydrocarbons, especially toluene.8 The cardiac involvement is relatively mild, does not have a fulminant course as in this patient, and does not progress after removal of the inciting agent. Glue sniffing cannot explain his illness. We do not have a history of alcohol intake heavy enough to explain this degree of cardiac dysfunction. Cocaine can cause a severe cardiomyopathy,9 but this diagnosis cannot be established without better evidence for chronic use.
Two collagen-vascular diseases, systemic lupus erythematosus and polymyositis, may prominently affect the myocardium. Myocardial involvement in lupus is a relatively small part of the illness, and given the paucity of other findings, I will exclude it. With respect to polymyositis, it is helpful to review the accepted case definition.10 There must be symmetrical progressive proximal muscle weakness, myositis by biopsy or electromyogram, and elevated creatine phosphokinase. I presume the creatine phosphokinase was not reported for this patient because it was not elevated. I am therefore excluding the diagnosis of polymyositis.
Lymphocytic myocarditis has clinical features similar to those of viral myocarditis. The clinical course is one of relatively slow progression, and improvement is frequent. The patient under consideration had a rapid downhill course atypical for this form of myocarditis, and I will therefore exclude it. Giant cell myocarditis is more difficult to exclude, and I will return to it.
Among the infectious causes, rickettsial diseases are all associated with systemic vasculitis.11 Therefore, in the absence of skin findings, I think we can exclude typhus, Rocky Mountain spotted fever, and Q fever. The myocarditis associated with chlamydial pneumonia12 is a minor feature of the illness. In our patient, cardiac involvement was the prominent feature and the right lower-lobe infiltrate a minor feature.
Spirochetal infection can cause myocarditis, as in Lyme disease. I shall exclude this diagnosis because heart block is such a prominent feature of Lyme carditis.13
Bacteria can cause myocarditis indirectly. There are three good examples of this: toxic shock syndrome,14 acute rheumatic fever,15 and diphtheria.16 In the absence of skin findings, I cannot make a diagnosis of toxic shock. The other two diagnoses I cannot exclude without further discussion.
We all know
viruses cause myocarditis (Table 2
). I think the
patient's
clinical course was entirely consistent with myocarditis caused
by coxsackievirus or echovirus,17 but this far into his
illness, negative titers exclude those diseases. There are only a few
other viruses worth discussing. Influenza virus can cause a
myocarditis.18 Although some of the clinical features of
influenza, such as fever and myalgia, were present, the
characteristic prostration seen with influenza was not described. This
negative finding is sufficient in my mind for excluding the diagnosis.
Hepatitis B has been associated with a fulminant
myocarditis,19 but that diagnosis is excluded by negative
serologies. Hantavirus is worth mentioning at this point because the
patient came from the Four Corners region, where cases of an acute
fatal respiratory illness were reported. In the series of Duchin et
al,20 myocardial involvement was not reported even at
autopsy. It is possible that the patient we are considering
represents the first case of hantavirus carditis, but, without
any of the known features of hantavirus infection, I cannot consider
that diagnosis at this point.
Thus far, I have excluded all but diphtheria, acute rheumatic fever, and giant cell myocarditis. I will also stray from being rigidly logical here and add hemochromatosis. Although it is not a myocarditis, hemochromatosis is worth considering. One variant of this disease affects primarily men in their 20s and 30s and presents with severe heart failure and little involvement of other organ systems.21 I hope, however, that the liver biopsy was reviewed carefully enough to exclude this possibility, and I will not consider it further.
Diphtheric myocarditis is an acute metabolic cardiomyopathy caused by circulating extracellular toxins produced by the bacteria. Diphtheria toxin enters myocardial cells and inhibits protein synthesis, resulting in cell death. Cardiac involvement occurs in about 10% of patients with diphtheria.16 Heart block and ventricular arrhythmias are common. Epidemics have been reported in the United States, such as that in the Seattle area in the late 1970s among homeless alcoholic men. A survey published in 198522 reported the highest per capita incidence in South Dakota, followed closely by New Mexico and Arizona. This pattern was due to low immunization rates and poor living conditions among Native Americans in those states. The patient considered here was Native American and came from the Southwest. However, only one case of diphtheria was reported in the United States in 1994, and that was in Massachusetts in a child whose family refused to have him vaccinated for religious reasons.23 I could find no cases reported in 1995. This epidemiology is striking enough to exclude a diagnosis of diphtheria.
Could this patient have had acute rheumatic fever? It is possible. He had one major and two minor Jones criteria24 : carditis, arthralgia, and fever. We should, however, characterize the carditis a little more closely. The carditis of acute rheumatic fever is usually accompanied by a murmur, but no murmur was noted in this patient. Massell et al25 identified 36 patients with congestive heart failure during a first attack; all had significant murmurs. Feinstein and Spagnuolo26 found significant murmurs in all 16 patients with congestive failure and acute rheumatic fever. More contemporary series of patients with rheumatic fever report Doppler echocardiographic findings; Veasy et al27 found valvular disease in 91%. I reviewed this patient's echocardiogram. It was a technically limited study, but it did not document mitral or aortic regurgitation. I am very troubled by the lack of a murmur. The lack of valvulitis leads me to exclude acute rheumatic fever at this juncture.
Giant cell myocarditis is an interesting disease increasingly recognized as a separate entity. The pathology is myocardial fiber degeneration with multinucleated giant cells present. It has an inevitably fatal course, with death usually occurring within 1 to 3 months. Davidoff et al28 reported on 10 patients diagnosed by biopsy. Compared with patients with other kinds of myocarditis, those with giant cell myocarditis had a significantly greater decline in left ventricular ejection fraction with time. Two patients died of cardiogenic shock. Nine had recurrent ventricular tachycardia, and seven had conducting system disease. The lack of ventricular arrhythmias or conducting system disease makes me very skeptical that the patient in question had giant cell myocarditis. The fact that our patient was significantly younger than the reported average age in the Boston series is supporting evidence against the diagnosis of giant cell myocarditis.
I now return to rheumatic fever, for several reasons. First, the entity of rheumatic pneumonitis explains some things that until this point I have neglected, especially presentation with hemoptysis and an abnormal chest radiograph. There has been controversy about whether or not rheumatic fever can cause a pneumonitis, with many authors believing that the lung pathology results from congestive heart failure or from superimposed infection. A relatively recent case report29 describes a 14-year-old boy with well-documented acute rheumatic fever. He also had a bilateral alveolar pattern on chest radiograph and respiratory failure. A right heart catheterization and a multigated acquisition scan demonstrated normal left ventricular function and normal filling pressures, excluding heart failure as a cause of the infiltrates. The authors carefully excluded infection. A short course of prednisone produced dramatic improvement within days.
Among the diagnoses considered so far, rheumatic fever best explains severe cardiac involvement with mild pulmonary involvement. The severe myocardial involvement without endocardial involvement may not be quite as difficult to explain if we consider the entity of recurrent rheumatic fever. Feinstein and Spagnuolo26 document that recurrent disease is more common in patients with carditis, and the severity of cardiac disease in recurrence depends on the severity of the previous attack. It may be that a patient with myocarditis on initial attack developed a more severe myocarditis as a result of recurrent disease without having developed endocarditis. Equally possible is that the murmur was not present initially but developed later in the course and is not mentioned in the case summary or was not picked up in this era of "hands off" intensive care medicine.
Bland and Jones30 looked at 306 fatal cases of rheumatic fever occurring during the period 1921 to 1937. Their observations are strikingly parallel to the case we are considering. Evidence of lung involvement other than that due to congestive heart failure was observed in 28% of patients during their final illness. Fatal cases typically had striking changes in the liver, both clinically and pathologically. Microscopic examination revealed widespread destruction of hepatic cells in the central portion of the lobules out of proportion for the degree of associated congestion.
The epidemiology is important. Although a recent series28 from Utah describes patients mostly from middle-class backgrounds, rheumatic fever is primarily a disease of poor living conditions. Although we do not know the specifics of the patient's social situation, the prevalence of poverty among Native Americans is high.
What do I think the autopsy will show? I think this patient had acute recurrent rheumatic fever with cardiac failure and rheumatic pneumonitis. The presence of Aschoff bodies would be reasonable evidence in support of the diagnosis. I think the patient also had ATN, acute hepatocellular necrosis, and bilateral adrenal hemorrhage, all resulting from heart failure. I cannot exclude several other diagnoses, especially giant cell myocarditis, but I think these are far less likely.
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Pathological Discussion |
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TopCase Presentation Clinical Discussion Pathological Discussion Final Diagnosis References |
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Dr Kevin S. Smith
A complete autopsy was performed approximately 3 hours after the declared time of death. External examination of the body showed marked jaundice and scleral icterus with evidence of therapeutic interventions but no sign of trauma. The heart weighed 375 g and externally showed a prominent right ventricle. The right ventricular wall was mildly thickened at approximately 5 mm. The right atrium was moderately dilated. The endocardial surfaces were smooth on inspection. Valvular vegetations or other structural abnormalities were not present. The coronary arteries were patent and elastic, and the intima was tan-yellow.
Histological sections of the left ventricle
and mitral
valve revealed discrete, widely scattered granulomatous lesions in a
perivascular distribution between fascicles of cardiac myocytes. These
microscopic lesions represent nearly classic forms of Aschoff
nodules (Figs 2 and 3).
Immunohistochemical staining to demonstrate macrophages was
strongly positive in the peripherally based Aschoff giant
cells and Anitschkow cells (Fig 4). The Anitschkow
cells, anecdotally thought to represent degenerated cardiac
myocytes, are more likely histiocytic cells, since immunohistochemical
staining for muscle-specific actin is negative in these
cells.31 32 In addition, dense infiltrates of chronic
inflammatory cells were seen in an endocardial distribution within the
mitral valve. Subsequent analysis of premortem plasma confirmed
an elevated anti–streptolysin O antibody titer at 391 IU/mL, with
the normal range 0 to 200 IU/mL.
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Gross and microscopic features of multiorgan failure were also confirmed. The liver showed extensive centrilobular congestion with necrosis, acute inflammation, and cholestasis. Diffuse, organizing alveolar damage was present throughout the pulmonary parenchyma. In addition, the lungs showed bilateral, focal lower-lobe infarcts with associated hemorrhage. Silver staining of tissue section in the regions of infarction demonstrated Candida species. Severe chronic passive congestion of small vessels within the cortices and vasa recta of the kidney was apparent.
Dr Havranek. Were the adrenal glands examined?
Dr Smith. They were normal.
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Final Diagnosis |
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TopCase Presentation Clinical Discussion Pathological Discussion Final Diagnosis References |
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Rheumatic myocarditis, with alveolitis consistent with rheumatic pneumonitis.
ATN and hepatic congestion due to cardiac failure.
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Selected Abbreviations and Acronyms |
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Footnotes |
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This clinicopathological conference was presented at the University of Colorado Health Sciences Center on May 5, 1995.
Received July 31, 1995; revision received September 28, 1995; accepted September 28, 1995.
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References |
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TopCase Presentation Clinical Discussion Pathological Discussion Final Diagnosis References |
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