Manuel Ramirez-Lassepas

Neurologic prognosis after cardiopulmonary arrest III. Seizure activity

Nineteen (30%) of 63 adult survivors of cardiopulmonary arrest had seizures after admission to the hospital. Eleven of 19 had more than one type of seizure. Myoclonic seizures began within 12 hours of the arrest in eight patients, and after 3 or more days in four patients. Only two (17%) patients with myoclonic seizures survived. Partial seizures usually began within 12 hours of the arrest and were controllable with anticonvulsants; 4 of 12 patients survived. Two of four patients with generalized tonic-clonic seizures survived; one of four with “shivering” lived. Overall, patients with seizures had a survival rate of 32% (6 of 19), compared with 43% for patients without seizures. None of the survivors had recurrent seizures within 6 months after hospital admission.

Neurologic prognosis after cardiopulmonary arrest; II. Level of consciousness

Sixty-three patients with isolated global anoxic-ischemic injury were prospectively evaluated after cardiopulmonary arrest (CPA); 25 (40%) survived, 16 to an excellent recovery, 8 to a good recovery, and 1 with severe deficits. Forty-six percent of the patients achieved full alertness, and only patients who did so survived. Seventy-five percent of patients arousable or initially alert (level of consciousness [LOC] ≥ 4) survived, all but two with excellent outcomes. Twenty-eight percent of patients initially in deep coma (LOC ≤ 3) survived, all with excellent or good outcomes. Ninety percent of patients who became fully alert did so within 72 hours. The likelihood of alerting is correlated with the LOC at given intervals after CPA. Reliable predictions of survival and outcome can often be based upon LOC alone within 2 days after CPA.

Neurologic status and prognosis after cardiopulmonary arrest I. A retrospective study

A retrospective survey of survivors of cardiorespiratory arrest included 34 patients. Twenty-one had a good outcome neurologically and 13 were seriously impaired. Depth and duration of postarrest coma correlated significantly with poor neurologic function. Seventy percent of the seriously impaired patients never regained consciousness and none emerged from coma within 5 days; 90 percent of patients with good outcome were alert within 18 hours after resuscitation. Coma, motor unresponsiveness, absent pupillary light reflexes, and absent oculocephalic responses were closely associated with dismal prognosis for neurologic functioning. This retrospective study cannot provide a basis for discontinuation of life support at any specific time.

Heparin-associated thrombocytopenia: A prospective evaluation of 211 patients

Two hundred eleven consecutive patients treated for acute thromboembolic disease were evaluated prospectively for the incidence of thrombocytopenia while receiving heparin treatment. One hundred patients received beef lung heparin and 111 patients received porcine intestinal mucosal heparin. All patients received a minimum of 4 consecutive days of continuous intravenous heparin, and platelet counts were determined prior to, at least twice weekly, and at the cessation of heparin therapy. Heparin-associated thrombocytopenia was defined as a decline from a normal platelet count (100,000-400,000/mm3) to less than 100,000/mm3 with a return to above 100,000/mm3 after the discontinuation of heparin. Heparin-associated thrombocytopenia developed in 11 patients (5.2% incidence). Ten of the thrombocytopenic patients had received beef lung heparin and one received porcine mucosal heparin. Chi-square analysis of these data was significant (p = 0.007). Plasma from seven of nine thrombocytopenic patients demonstrated a plasma factor compatible with a heparin-sensitive antiplatelet antibody. Heparin-associated thrombocytopenia appeared on days 2 to 10 of therapy. Cessation of heparin resulted in remission of thrombocytopenia within 4 days in all patients. Serial quantitative platelet count determinations are indicated in all patients receiving therapeutic heparinization for the early recognition and resolution of heparin-associated thrombocytopenia.

Heparin‐induced thrombocytopenia in patients with cerebrovascular ischemic disease

We studied 137 patients who were treated with heparin for cerebral infarction (73), partially reversible ischemic neurologic deficit (22), or transient ischemic attack (42). Platelet counts were performed before therapy, twice weekly, and at cessation of therapy. Platelets decreased in 118 patients (86%). In 21 (15.3%), platelets dropped ≥40%; 9 of 14 new ischemic events and three of six deaths occurred in this group of patients. Because there was a significant association between poor outcome and platelet drop ≥40% (p < 0.001), we believe that platelets should be monitored frequently when patients are treated with heparin for ischemic cerebrovascular disease.

Antifibrinolytic therapy in subarachnoid hemorrhage caused by ruptured intracranial aneurysm

There are 25 published studies on the treatment with antifibrinolytic agents of subarachnoid hemorrhage (SAH) caused by ruptured intracranial aneurysm. Twelve of these studies were uncontrolled and, except for one, all reported reduced incidence of rebleeding. Of 13 controlled studies, 9 were randomized, and 3 were also double-blind. In 7, reported decrease in rebleeding was reported, but only 4 showed decreased mortality. Three studies showed no effect, and three reported a higher incidence of rebleeding in treated patients. Discrepancies may be due to the multiple clinical variables of SAH and to flaws in methodology; nevertheless, the data fail to demonstrate that antifibrinolytic therapy alters the natural history of the disease.

Heparin therapy for stroke Hemorrhagic complications and risk factors for intracerebral hemorrhage

Hemorrhages occurred in 16 (3.1%) of 510 patients treated with continuous intravenous heparin for acute cerebral infarction(269), reversible ischemic neurologic deficit (81), or transient ischemic attack (160). Three patients (0.6%) had intracerebral hematomas. Riskfactors included abnormal CT within 24 hours of onset of symptoms (3.2%), severe neurologic deficit (2.8%), two acute infarcts by CT (2.1%), known source of embolus (1.3%), and final diagnosis of cerebral infarction (1.1%). The only identifiable risk factor for systemic hemorrhage (GI LO%, GU 0.8%, muscle 0.4%, skin 0.1%) was age over 60 years. The incidence of intraspinal hematoma was 0.6%. Two of the intracerebral hematomas were fatal, and mortality was 31% in patients with hemorrhagic complications; however, the risk of CNS hemorrhage was only 0.8%.

A new model of experimental cerebral infarction in New Zealand white rabbits

SummaryTo develop an easy, reproducible experimental model of cerebral infarction (CD without craniotomy in New Zealand white rabbits, a silicone rubber cylinder embedded in a nylon suture was delivered to the middle cerebral arteries through the internal carotid artery in anesthetized animals. Rabbits were sacrificed 0. 5 –5 h after embolization. CI size and location were ascertained by the triphenyl–2H-tetrazolium chloride (TTC) staining method; cerebral blood flow (CBF) was measured prior to and after embolization. in all rabbits after 4 h of ischemia, in 50 % after 3 h and only in 33 % after 2. 5 h. CI did not occur within less than 2. 5 h of ischemia. No correlation was found between size and location of CI and occlusion time. CBF was maximally reduced in the fight MCA territory but was also reduced in both anterior cerebral arteries and left MCA territories. This model is technically easy and the retrievable embolus allows the study of reperfusion by pulling on the nylon suture. It is suitable for studying chemical and molecular changes of the ischemic cells and/or for studying neuroimage changes after ischemic stroke.

Cardiorespiratory Arrest in Aneurysmal Subarachnoid Hemorrhage

Aneurysmal subarachnoid hemorrhage (ASAH) can cause sudden death from cardiorespiratory arrest (CRA). Successful resuscitation (SR) allows diagnosis and treatment of survivors. We studied incidences of CRA and the influence of SR in ASAH prognosis. Hospital records of patients with ASAH diagnosed by computed tomography, lumbar puncture, surgery, or autopsy and treated from 1980 to 1988 were reviewed. Symptoms, aneurysm location, treatment, course, and outcome were tabulated. The literature was reviewed. Of 95 consecutive ASAH patients, 15 (16%, 2 males, 13 females) had CRA, seven primary cardiac, six primary respiratory, and two combined CRA. Four of 11(36.4%) had posterior circulation aneurysm (PCA);13 (86.6%) had intracerebral-ventricular clot (ICC). All were clinically Stage V, six improved and had angiography, two had surgery, and one (7%) survived hospitalization. Of other ASAH patients (37 males and 43 females), 4.4% of 68 had PCA, 37.5% had ICC, and 56% survived hospitalization. Of 287 patients hospitalized after out-of-hospital SR in the same period, 18% survived; 14 (4.9%) had ASAH and 1 (7%) survived hospitalization. CRA is not infrequent after onset of ASAH and occurs more commonly in women with PCA. Most likely, it is due to a very large initial hemorrhage disrupting diencephalic circulatory and respiratory centers. Prognosis of patients suffering CRA from ASAH is dismal and not influenced by SR.

Cervical myelopathy complicating cerebral angiography Report of a case and review of the literature

Transverse cervical myelopathy, at C-6 level, followed injection of Renografin-60 into the right thyrocervical trunk during cerebral angiography. Review of the literature yielded only two cases in which attempted posterior fossa angiography resulted in cervical myelopathy. Two more cases were found. In one, cervical myelopathy occurred during aortography in a patient with coarctation of the aorta, and in the other it followed mediastinal angiography. Summation of anoxia, hemorrhage, and cellular toxicity is responsible for spinal cord necrosis following arterial injection of contrast material.