|LETTER TO EDITOR
|Year : 2012 | Volume
| Issue : 1 | Page : 35-36
A silent thunder clap!
Dilip Gude1, Dharam Pal Bansal2
1 Department of Internal Medicine, Medwin Hospital, Nampally, Hyderabad, AP, India
2 Department of Pulmonology and Critical Care, Medwin Hospital, Nampally, Hyderabad, AP, India
|Date of Web Publication||21-May-2012|
AMC, 3rd Floor, Medwin Hospital, Chirag Ali lane, Nampally, Hyderabad - 500 001, AP
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gude D, Bansal DP. A silent thunder clap!. Int J Health Allied Sci 2012;1:35-6
Subarachnoid hemorrhage (SAH) presenting without headache is quite uncommon. We would like to share one such a presentation. A 30 yr old hypertensive and nondiabetic male, ethanolic (consuming about 60 g of ethanol per day) and an occasional smoker, presented with history of giddiness followed by a fall from the chair. Patient then had generalized tonic clonic seizures lasting for about a minute following which he had post-ictal confusion. Patient was diagnosed of hypertension 4 years ago but has been noncompliant for medication use. There was no history of headache before or after the event. His blood pressure was 220/120 mm of Hg. Patient was restless and agitated although there was no focal neurological deficit appreciable in the patient. Patient's restlessness improved up on sedation (midazolam 2 mg) and levetiracetam (1 gm loading dose and 500 mg TID). Neck rigidity was characteristically absent. Examination of other systems was normal. CT scan of the brain showed subarachnoid hemorrhage [Figure 1]. Lumbar puncture demonstrated high opening pressure and plenty of RBC and xanthochromia. ECG showed left ventricular hypertrophy by voltage criteria. Nimodipine was started at 60 mg thrice daily and later reduced to 30 mg twice daily. Intravenous nitroglycerin infusion was titrated as per his blood pressure. His sensorium improved remarkably and was coherent and fully oriented. He began complaining of severe pain in right upper limb. X-ray showed an anterior dislocation of the right shoulder which was managed by reduction, immobilization and NSAIDs. Most causes of secondary hypertension were ruled out. Negative drug history, Normal sized kidneys (on ultrasonography), absence of renovascular hypertension (normal duplex), 2D echo ruling out coarctation of aorta, and negative urinary metanephrines point the aetiology to essential hypertension. Although strongly recommended further hospital stay, the patient voluntarily chose to get discharged despite our elaborating his high risk.
|Figure 1: Noncontrast CT showing interhemispheric subarachnoid blood (Fisher scale Group-2)|
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The unique aspect of this presentation is the striking absence of headache. A study on 224 patients of SAH depicted that the percentage of SAH presenting without headache is 8%. Also that group did not sport any specific clinical characteristics different from those who had headache.  Another case-report described SAH without headache but with meningismus.  A school of thought argues that amnesia for the event may explain the purported absence of headache which may be the case in our case (post-ictal state).  The risk factors for SAH in our patient are his uncontrolled hypertension, moderate to heavy alcohol intake and smoking. Although classically seizures have been related to the occurrence of posterior dislocation, our case had an anterior dislocation. Our patient's age (30 years) is also not typical as 80% of cases of SAH occur in people aged 40-65 years. 
In a study the rate of initial misdiagnosis was 12 percent and it was independently associated with small SAH volume, normal mental status at presentation, and right-sided aneurysm location. Initial normal mental status accelerated the misdiagnosis rate to 20 percent and was associated with a nearly four-fold increase in mortality at 12 months as well as increased morbidity among survivors. 
Our case highlights the importance of understanding the atypical manifestations of a deadly entity- SAH and reiterates that knowledge about the same enables the clinician to not just better manage but brace up to deal with the dreaded complications.
| Acknowledgments|| |
We thank the department of internal medicine and pulmonology/critical care for their perpetual support.
| References|| |
|1.||Naganuma M, Fujioka S, Inatomi Y, Yonehara T, Hashimoto Y, Hirano T, et al. Clinical characteristics of subarachnoid hemorrhage with or without headache. J Stroke Cerebrovasc Dis 2008;17:334-9. |
|2.||Weissman MN. Atypical presentation of subarachnoid hemorrhage: Case report and review of the literature. WMJ 2002;101:47-50. |
|3.||Becske T, Jallo G. Subarachnoid hemorrhage. www.emedicine.com. Available from: http://emedicine.medscape.com/article/1164341-overview [Last accessed on 2012 Feb 02]. |
|4.||Kowalski RG, Claassen J, Kreiter KT, Bates JE, Ostapkovich ND, Connolly ES, et al. Initial misdiagnosis and outcome after subarachnoid hemorrhage. JAMA 2004;291:866-9. |