(Circulation. 1995;91:3017-3019.)
© 1995 American Heart Association, Inc.
Articles |
Sudden Loss of Consciousness, Dyspnea, and Hypoxemia in a Previously Healthy Young Man
From the Departments of Internal Medicine (H.L.F.) and Pathology and Laboratory Medicine (M.Y.), the University of Texas Medical School at Houston, the University of Texas at Houston Health Science Center.
Correspondence to Herbert L. Fred, MD, St Luke's Episcopal Hospital, 6720 Bertner Ave, Room B524 (MC1-267), Houston, TX 77030-2697.
 |
Introduction |
|---|
 Top Introduction Case Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
|
Case Presentation |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
A previously healthy 37-year-old man had a sudden syncopal episode that lasted an estimated 10 seconds. The patient's wife, who witnessed the event, said that his eyes rolled back and that he urinated but had no tonic-clonic activity. On regaining consciousness, he complained of dizziness, shortness of breath, and sweating. An emergency medical service then brought him to the hospital.
In the emergency department, the patient complained of shortness of breath but denied chest pain, cough, fever, headache, weakness, or previous neurological difficulty. He had no significant past medical history and had been well before losing consciousness.
On physical examination, the patient was alert and oriented but anxious and dyspneic. His oral temperature was 99°F; pulse, 115 bpm and regular; blood pressure, 105/70 mm Hg; and respirations, 20 breaths per minute. Cranial nerve function and optic fundi were normal. Neck veins were not distended, and the precordium was quiet, with normal heart sounds and no murmurs. Lungs were clear to auscultation. Abdominal findings were unremarkable, and the extremities had full, equal pulses with no edema.
The chest radiograph and ECG obtained at entry appear in Figs
1
and 2, respectively. Arterial blood gas
analysis (room air) disclosed a pH of 7.46, a
PaCO2 of 30 mm Hg, a
PaO2 of 52 mm Hg, and an O2
saturation of 89%. Results of the following laboratory studies were
normal: complete blood count; urinalysis; serum creatinine, calcium,
phosphorus, and electrolytes; blood sugar and urea nitrogen; and liver
function tests.
|
|
The patient remained dyspneic but stable for 5 hours; then suddenly, while awaiting admission for workup of "new-onset seizures," he lost consciousness again. This time he had tonic-clonic activity of both upper extremities. The pulse oximeter showed a saturation of 86%, and a repeat chest radiograph demonstrated no significant change. Shortly thereafter, asystole developed. During vigorous resuscitative efforts, the patient received a 20-mg IV bolus of TPA, followed minutes later by a 60-mg bolus. All measures proved fruitless, and 6 hours after his illness began, the patient died.
|
Clinical Commentary |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
Herbert L. Fred, MD
I first learned of this patient when I came across his autopsy report. Consequently, I know the final diagnosis. Nevertheless, the history in this case, coupled with the initial clinical and laboratory findings, should have suggested the correct diagnosis immediately. Ask yourself this question: What could cause a perfectly healthy young man to experience sudden transient loss of consciousness, followed closely by persistent dyspnea and hypoxemia, all in the absence of demonstrable cardiac or pulmonary parenchymal disease? The answer, of course, is PTE. And if we add rapid death to the mix, the answer becomes massive PTE. Before commenting further, I think it would be best to see the autopsy findings.
|
Pathological Findings |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
Mary Yang, MD
Autopsy was performed 25 hours after death. The significant pathological findings were in the lungs. A large saddle embolus was present at the bifurcation of the main pulmonary trunk with extension into and obstruction of the right and left main pulmonary arteries (Fig 3
). Histological sections of the embolus
showed a blood clot with tangled strands of fibrin and focal attachment
to the arterial wall (Fig 4).
|
|
Other findings in the lungs included bilateral pulmonary congestion and focal intra-alveolar hemorrhage. Emboli were also present in the small segmental branches of the pulmonary arteries. No pulmonary infarct was identified. Careful examination of the cardiac chambers, vena cava, iliac veins, femoral veins, and periprostatic venous plexus revealed no source for the emboli.
Other important incidental findings included cardiomegaly (heart weight, 580 g) with concentric left ventricular hypertrophy and focal atherosclerosis of the left coronary artery. The atherosclerotic plaque in the left coronary artery severely occluded the lumen of the anterior descending branch and the orifice of the circumflex branch. Findings in other organs were unremarkable.
|
Clinical Discussion |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
Herbert L. Fred, MD
Although the medical literature is replete with articles on PTE, it offers little information on the neurological manifestations of this disease. That deficit has particular relevance to the case under discussion, because a neurological event signaled both the onset and end of the patient's rapidly fatal clinical course. Therefore, I will focus my comments almost entirely on the neurological aspects of PTE.
Of the many different neurological manifestations of PTE, the most frequent are restlessness, anxiety, syncope (at rest or on effort), focal or generalized seizures, altered mental state (including stupor and coma), and weakness or paralysis of limbs (eg, monoparesis, hemiparesis, and hemiplegia). Other occasional manifestations are ocular palsies, transient cortical blindness, dysarthria, aphasia, ataxia, hiccups, fecal or urinary incontinence, and an overpowering urge to defecate.1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18
The pathogenesis of these signs and symptoms remains speculative. In many if not most cases, hypoxia of the brain undoubtedly plays a major role. Such hypoxia results from decreased cardiac output consequent to arrhythmias, mechanical obstruction of the pulmonary arteries, or both. The hypoxic effects probably depend on the rapidity of onset as well as the degree and duration of decreased systemic blood flow.19 These effects presumably are more pronounced in the presence of preexisting brain disease, especially atherosclerosis.1 7 Careful histological study, however, does not always provide adequate explanation for all of the premortem neurological abnormalities, particularly the lateralizing signs.15 19
Rarely, two other pathogenetic mechanisms come into play. Thrombosed pulmonary veins lying adjacent to or within a segment of infarcted lung are a potential source for cerebral emboli.20 And, of thrombi originating in systemic veins, some lodge in the lungs, while others reach the brain through intracardiac21 or intrapulmonary22 shunts (paradoxical emboli).
The incidence of these neurological manifestations is hard to determine. Most authors either do not mention neurological findings or simply list them as part of the diverse clinical expressions of PTE. Others refer only to the frequency with which neurological syndromes predominate. For example, mental symptoms occur in up to 60% of patients,13 but neurological manifestations are major findings in only 5% of patients.4 7 23
Neurological manifestations of PTE generally appear in elderly, bedridden, and cardiac patients. They usually are abrupt in onset and often are transient and recurrent (how many TIAs are, in fact, PTE?). And they can be the first,2 4 5 9 13 15 16 the most prominent,1 3 4 7 15 16 23 or virtually the only4 manifestation of PTE.
Differential diagnostic possibilities are numerous24 and depend mainly on the clinical circumstances in a given case. When neurological signs predominate, the diagnosis frequently is CVA4 5 6 9 15 23 and sometimes brain tumor.3 This mistake is understandable, because primary brain disease can also cause labored respirations, ECG changes,25 and pulmonary parenchymal infiltrates.26 Thus, clinical differentiation of PTE from a CVA (and from a TIA) can be more difficult than one might think.
Cardiac disease is the other common misdiagnosis. Recurrent syncopal episodes can mimic Stokes-Adams attacks.2 15 Chest pain usually suggests myocardial infarction15 23 and occasionally, dissecting aortic aneurysm.27 Consequently, when acute cardiorespiratory and neurological abnormalities coexist, one should routinely consider PTE as well as Stokes-Adams attacks, myocardial infarction, and dissecting aortic aneurysm.
In closing, I want to emphasize two points: (1) Today's case is a chilling reminder that PTE can strike, and sometimes kill, young people—even those who are seemingly healthy, have no identifiable risk factors, and are free of detectable underlying disease.28 (2) Today's case also reminds us that almost all patients with this life-threatening illness live long enough to have appropriate diagnostic studies and to receive proper therapy.
|
Final Diagnosis |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
Massive pulmonary thromboembolism.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Footnotes |
|---|
This clinicopathological conference was presented at Lyndon B. Johnson General Hospital, Houston, Tex, February 22, 1995.
|
References |
|---|
|
TopIntroductionCase Presentation Clinical Commentary Pathological Findings Clinical Discussion Final Diagnosis References |
|---|
1. Hussey H, Katz S. Pulmonary embolism. GP. 1955;12:59-68.
2. Case records of the Massachusetts General Hospital. N Engl J Med. 1963;268:371-378.
3. Hamilton M, Thompson EN. Unusual manifestations of pulmonary embolic disease. Postgrad Med J. 1963;49:348-353.
4. Miller R, Berry JB. Pulmonary infarction: a frequently missed diagnosis. Am J Med Sci. 1951;222:197-206. [Medline] [Order article via Infotrieve]
5. Roth IR. Differential diagnostic problems in acute pulmonary embolization. Am J Med. 1948;4:493-502. [Medline] [Order article via Infotrieve]
6.
Sagall EL, Barnstein J, Wolff L. Clinical
syndrome in patients with pulmonary embolism. Arch Intern
Med. 1945;76:234-238.
7. Israel HL, Goldstein F. The varied clinical manifestations of pulmonary embolism. Ann Intern Med. 1957;47:202-226.
8. Hickam JB, Sieker HO. Pulmonary embolism and infarction. DM. Jan 1959;1-36.
9. Fowler EF, Bollinger JA. Pulmonary embolism: a clinical study of ninety-seven fatal cases. Surgery. 1954;36:650-663. [Medline] [Order article via Infotrieve]
10. Ehrner L, Garlind T, Linderholm H. Chronic cor pulmonale following thromboembolism: a clinical and pathophysiological study of three cases. Acta Med Scand. 1959;164:279-297. [Medline] [Order article via Infotrieve]
11. Ramirez LM. Thromboembolic disease in adolescence. JAMA. 1959;170:1808-1811.
12. Costeas F, Raftopoulos J, Liarakos E. Cerebral stroke immediately following pulmonary embolism. Angiology. 1965;16:355-357.
13. Krause S, Silverblatt M. Pulmonary embolism: a review with emphasis on clinical and electrocardiographic diagnosis. Arch Intern Med. 1955;96:19-25.
14. Gerber IE. Pulmonary embolism in the aged: unusual clinical features. Geriatrics. 1964;19:3-10.[Medline] [Order article via Infotrieve]
15.
Fred HL, Willerson JT, Alexander JK.
Neurological manifestations of pulmonary
thromboembolism. Arch Intern Med. 1967;120:33-37.
16.
Thames MD, Alpert JS, Dalen JE. Syncope in
patients with pulmonary embolism. JAMA. 1977;238:2509-2511.
17.
Busch U, Renner U, Wirtzfeld A, Sebening H, Klein G,
Hagl S. Floating pulmonary embolus: unusual cause of recurrent
syncope. Eur Heart J. 1984;5:602-605.
18. Stiller RJ, Leone-Tomaschoff S, Cuteri J, Beck L. Postpartum pulmonary embolus as an unusual cause of cortical blindness. Am J Obstet Gynecol. 1990;162:696-697. [Medline] [Order article via Infotrieve]
19.
Adams JH, Brierley JB, Connor RCR, Treip CS. The
effects of systemic hypotension upon the human brain: clinical and
neuropathological observations in 11 cases. Brain. 1966;89:235-268.
20.
Wallach R, Pomerantz N, DiMaio D. Emboli arising
in the lungs. Arch Intern Med. 1957;99:142-146.
21.
Biller J, Adams HP Jr, Johnson MR, Kerber RE, Toffol
GJ. Paradoxical cerebral embolism: eight cases.
Neurology. 1986;36:1356-1360.
22.
Sisel RJ, Parker BM, Bahl OP. Cerebral symptoms
in pulmonary arteriovenous fistula: a result of paradoxical
emboli(?). Circulation. 1970;41:123-128.
23. Gorham LW. A study of pulmonary embolism, I: a clinicopathological investigation of 100 cases of massive embolism of the pulmonary artery; diagnosis by physical signs and differentiation from acute myocardial infarction. Arch Intern Med. 1961;108:8-22.
24. Fred HL, Peterson KL. Differential diagnosis of acute pulmonary thromboembolism. GP. 1969;39:78-89.
25.
Surawicz B. Electrocardiographic pattern of
cerebrovascular accident. JAMA. 1966;197:913-914.
26. Richards P. Pulmonary oedema and intracranial lesions. Br Med J. 1963;2:83-86.
27. Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine. 1958;37:217-279. [Medline] [Order article via Infotrieve]
28. Loehry CA. Pulmonary emboli in young adults. Br Med J. 1966;1:1327-1328.
This article has been cited by other articles:
 |
|
 |
|
  A K Shah and M Darwent Acute pulmonary embolism presenting as seizures Emerg. Med. J., April 1, 2009; 26(4): 299 - 300. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||