Objective: Aimed to asses the role of PT estimation in early diagnosis and predicting the extent and the outcome of head injury with ICerH and/ or Contusion
Method :PT was measured by Digiclot 818
Group –1: One hundred consecutive head injured patients admitted at Neurosurgical and Al Ramadi teaching hospitals were initially estimated for prothrombin time and subsequently scanned
Group-2 : Two hundred twenty five consecutive non scanned head injured patients admitted to Neurosurgical and Al Ramadi teaching hospitals were estimated with prothrombin time at the time of insult and subsequently for the next two weeks Al – Kindy Col Med J 2012; Vol. 8 No. 1 P: 54
Clinical and neurological evaluation (GCS) score in addition to computerized tomography scan was done for both groups
Result :Group -1: Twenty eight (28%) of the initially estimated head injured patients had prolonged prothrombin time in which their subsequent CT scan revealed an ICer H and/or contusion
Seventy six (76%) percent of those with severely head injured patients (GCS≤8) were having an initial prothrombin time prolongation..While those with mild head injury (GCS≥12) only thirty (30%) of them were having the initial prothrombin time prolongation
Group-2 Those patients who survived the initial insult and subsequently thereafter (surgically or conservatively treated) even with a deficit.. Daily estimation of prothrombin time showed a decline within the 7-14 days
Those patients who finally died (surgically or conservatively treated) daily estimation of prothrombin time showed a persistent elevation or a fluctuation within the next 7-14 day
Conclusion Prothrmbin time is an important
parameter in :
1-Reflecting the severity of head injury (GCS)
3-Early detection of ICerH and /or contusion
2-Prognostic value in cases of of ICerH and /or contusion
Abb : ICerH = Intracerebral hematomas,SDH=subdural hematomas,EDH=epidural hematomas,SAH=subarachnoid hemorrhages,PT=Prothrombin time,Pts=Patients,CT scan=computarized tomography.
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Exposure to lead results in significant accumulation in most of vital organs, and free radical damage has been proposed as a cause of lead-induced tissue damage, where oxidative stress is a likely molecular mechanism. This study was designed to evaluate therapeutic effects of melatonin in lead-induced organ toxicity in rats. The therapeutic effects of melatonin on lead induced toxicity in rats were evaluated using 36 rats, which were allocated into 3 groups and treated as follows: Group I, includes 12 rats injected subcutaneously with 0.2 ml physiological saline for 30 days, followed by treatment with a daily dose of 20mg/kg melatonin, administrated I.P for the successive 30 da
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