Madhavi Bollu

ACUTE ABDOMINAL AORTIC THROMBOSIS AS A COMPLICATION OF THE HEIMLICH MANEUVER

1. Shaw PJ, Walls TJ, Newman PK et al. Hashimoto’s encephalopathy: A steroidresponsive disorder associated with high anti-thyroid antibody titers-report of 5 cases. Neurology 1991;41:228–233. 2. Azuma T, Uemici T, Funaucghi M et al. Myelopathy associated with Hashimoto’s disease. J Neurol Neurosurg Psychiatry 2000;68:679–683. 3. Chong JY, Rowland LP, Utiger RD. Hashimoto encephalopathy: Syndrome or myth? Arch Neurol 2003;60:164–171. 4. Ferracci F, Bertiato G, Moretto G. Hashimoto’s encephalopathy: Epidemiologic data and pathogenetic considerations. J Neurol Sci 2004;217:165–168. 5. Ferlazzo E, Raffaele M, Mazzu I et al. Recurrent status epilepticus as the main feature of Hashimoto’s encephalopathy. Epilepsy Behav 2006;8:328–330. 6. Nolte KW, Unbehaun A, Sieker H et al. Hashimoto encephalopathy: A brainstem vasculitis? Neurology 2000;54:769–770. 7. Duffey P, Yee S, Reid IN et al. Hashimoto’s encephalopathy: Postmortem findings after fatal status epilepticus. Neurology 2003;61:1124–1126. 8. Doherty CP, Schlossmacher M, Torres N et al. Hashimoto’s encephalopathy mimicking Creutzfeldt-Jakob disease: Brain biopsy findings. J Neurol Neurosurg Psychiatry 2002;73:601–602. 9. Perrot X, Giraud P, Biacabe AG et al. Hashimoto’s encephalopathy: An anatomicoclinical observation. Rev Neurol 2002;158:461–466. 10. Mahad D J, Staugaitis S, Ruggieri P et al. Steroid-responsive encephalopathy associated with autoimmune thyroiditis and primary CNS demyelination. J Neurol Sci 2005;228:3–5.

GELASTIC PRESYNCOPE: AN UNUSUAL MANIFESTATION IN AN ELDERLY PATIENT

CASE REPORT A 67-year-old man was seen in consultation for the complaint of near blackout spells with laughter. The first episode occurred while listening to a radio program while driving, when his laughing heavily resulted in blurring vision, darkening of visual field, feeling faint, and sensation of imminent loss of consciousness. He slowed his vehicle and pulled off the road, and the symptoms soon resolved. He denied complete loss of consciousness, uncontrolled movement of limbs, bowel or bladder incontinence, headache, or other associated symptoms. Since this index episode, patient reports recurrent episodes of near loss of consciousness associated with vigorous laughing. Episodes last only a few seconds. He had similar symptoms, but of lesser severity, in relation to straining during defecation and micturition. The patient denied any palpitations, irregular heartbeat, chronic cough, chest pain, shortness of breath, nausea or vomiting, diarrhea, other systemic or constitutional symptoms, having had stroke in the past, any history of seizures, or any sleep disturbances, including any symptoms suggestive of narcolepsy or cataplexy. His medical history was significant for diabetes mellitus, hypertension, and prolonged posttraumatic disorder, which were stable. The patient was evaluated using magnetic resonance imaging and a magnetic resonance angiogram of the brain, which showed only mild periventricular white matter changes that were nonspecific. Carotid Doppler studies were unremarkable. Chest X-rays were normal. No further diagnostic investigation was pursued because behavioral modification of avoiding vigorous prolonged laughter resolved his symptoms completely. DISCUSSION Gelastic presyncope or syncope is a relatively uncommon type of neurally mediated event with a drop in systemic vascular resistance due to arterial dilation in the setting of a relative or absolute bradycardia. During prolonged laughter, there is repetitive Valsalva effect with reduced venous return secondary to increased intrathoracic pressure with associated systemic arterial dilatation and bradycardia resulting in reduced cardiac output and cerebral hypoperfusion. If the Valsalva effort is not aborted during the presyncopal phase, it is likely that it will culminate in a syncopal episode. This mechanism is similar to that seen with cough syncope. In addition, emotional factors and cerebral vasoconstriction secondary to systemic hypocapnia could be contributing to the syncope in this situation. This patient also had presyncopal sensations to straining from defecation and urination, suggesting Valsalva effect as the most likely mechanism. Laughter or gelastic syncope can potentially be misdiagnosed as cataplexy related to laughter. There have been only a few case reports of laughter syncope previously reported, mostly in the elderly population, in healthy adults and people predisposed to dysautonomia. Possible contribution of dysautonomic neuropathy secondary to diabetes mellitus can not be excluded in the current patient. A more-serious underlying mechanism of severe vascular disease involving the brachiocephalic trunk was noted to be the mechanism in the first reported case of laughter syncope. Syncope resolved after percutaneous angioplasty. Falls in elderly people can lead to devastating consequences, and hence it is essential to diagnose and prevent syncope in this age group. Beta-blockers and midodrine were noted to have beneficial effects in controlling symptoms in one described case of neurally mediated syncope. Behavioral modification may be the best initial approach before exposing the patients to medications.

Transient Ischemic Attack in an Elderly Patient: What to Expect?

A 77-year-old man presented with an episode of facial droop, confusion, and profuse sweating that resolved en route to the emergency department. A computed tomography scan of the abdomen was ordered when on physical examination a palpable, pulsatile abdominal mass was noted. Computed tomography scan revealed a large infrarenal abdominal aortic aneurysm (AAA) with peripheral thrombus and a small, contained leak (Figure 1). Presentation of transient ischemic attack (TIA)-like symptoms prompted the medical evaluation in our patient, and, at that time, the incidental finding of the leak of the AAA was made. We believe that the hypotension caused by the AAA leak was responsible for the focal neurologic symptoms. TIA is regarded as a warning sign for stroke and can be precipitated by conditions that alter cerebral perfusion. Few previous reports in the literature focus on hypotension as a cause of TIA.1 Clinicians should be aware that episodes of hypotension followed by TIA-like symptoms could be caused by abnormalities of the endovascular system, such as AAA.

Cardiac Arrest After Percutaneous Transthoracic Needle Biopsy: A Consideration Other Than Pneumothorax!

CLINICAL PRESENTATION A 59-year-old man with a new right upper lobe nodule underwent a computed tomography-guided percutaneous biopsy with a 19-gauge biopsy needle. During the second needle pass, the patient coughed and then developed hemoptysis, prompting the procedure to be terminated. Evaluation of the patient’s postprocedure computed tomography scan, which was performed because of hemoptysis, showed the presence of air in the left ventricle and in the aorta (Figures 1 and 2). Imaging also demonstrated a moderate amount of pulmonary hemorrhage at the biopsy site and a small rightsided pneumothorax. He became unresponsive after the computed tomography scan with repeated bouts of pulseless electrical activity and a single episode of ventricular fibrillation. The patient was intubated, placed on high constant oxygen supplementation and also placed in the left lateral Trendelenburg position. He developed aspiration pneumonia and was eventually discharged home. The most frequent complications of percutaneous transthoracic needle biopsy include pneumothorax, hemorrhage and hemoptysis. The formation of a communication between an airway and a pulmonary vein is the presumed mechanism of air embolization resulting from percutaneous lung biopsy. Hyperbaric oxygen therapy is also currently regarded as a mainstay of therapy for affected patients, as it increases the rate of resorption of the embolized air.1,2 In conclusion, clinicians should be aware of this unusual complication after percutaneous lung biopsy, as early recognition leads to improved outcomes.

FALLS IN ELDERLY PEOPLE

to the very essence of Ockham. Ockham was a radical nominalist and held that any generalization away from the particular was a convenient fiction. To treat the complicated patient, we may have to return to the individuality of the patient before us. Each one will present a unique combination of medical, financial, social, and psychological realities to be addressed within the systematic framework of care that the team has available. The successful treatment of any will require all to be addressed.