Abstract:

In organophosphate poisoning (OFZ) cases, findings often occur associated with the excessive activity of the parasempathic nervous system. But sometimes findings associated with excess activity of the sympathic nervous system, such as hypertension and tachycardia, may also develop. Subaraknoid bleeding (SAK) is often secondary to aneurysm or arteriovenous malformation (AVM) rupture. However, in cases where the presence of aneurysma is not shown (e.g. associated with hypertensive hemorrhage) the development of SAK is also. Our goal is to discuss the relationship of SAK with OFZ in an event of OFZ. At the age of thirty to nine, the patient was concerned with a close loss of consciousness. In anamnese, it was discovered that he drinks 150 cc of organophosphate farm medicine. In the application, the Glasgow coma scale (GKS) score was 3 and rose to 11 after half an hour. Arterial pressure (TA) was 120/90 mm/hg, pulse 112/min and fever 37.2 ° C. The pupils were myotic (2mm/2mm), light reflection was weak. There was no focal neurological deficit and no findings of meningism were found. The blood cholesterol level (ChE) was measured at 121 u/L (3600-12000 u/L). 18 hours after the application, TA was 200/130 mm/hg. Meanwhile, the GKS score dropped to 4 and there were findings in the brain tomography (BT) compatible with SAK. The repeated serum ChE was 1908 u/L. In the 7th day, the patient had a cardiopulmonary arrest resulting in exit. Our case may indicate that in cases with OFZ, especially in severe cases, there may be a hypertensive crisis associated with the hyperactivation of the sympathic system and associated SAK. Subarachnoid hemorrhage in a Case with Organophospate Poisoning Althought the findings of involvement of the parasympatic nerve system are common in the patients with organophospate poisoning (OPP), findings such as hypertension associated with the sympatic hyperactivity may not often be established. Subarachnoid hemorrhage (SAH) often occurs due to the rupture of cerebral aneurysms or arteriovenous malformations (AVM). However it has been that SAH may also develop due to nonaneurysmal c a u s e s such as hypertensive hemorrhage. Our goal is to discuss the association with OPP of SAH in a case with OPP. A thirty-nine old man, presented with the loss of conscious. He ingested approximately 150 cc of a commercial formulation of dimethylamine. Glasgow coma scala (GCS) score was 3 on admission and was 11 thirty minutes later. Tension arterial (TA) was 120/900 mm/Hg, pulse rate was 112/minute, tempareture was 37.2 C°. Pupillaries were myotic (2 mm/ 2 mm) and unreactive to light. There was no focal norologic defisite including meningism findings. Blood cholinesterase (ChE) level was measured as 121 u/L (3600-12000 u/L). Eighteen hours after admission TA was 200/130 mm/Hg with GCS score of 4. Cranial computed tomography (CT) revealed SAH. Repeteated blood ChE level was 1908. He died as a result of cardiopulmonary arrest on day 7th. Our case may show SAH in association with hypertensive crisis due to sympatic hyperactivation in patients with OPP, especially in those with severe poisoning.