Diffuse Cerebral Edema Research Articles

Síndrome del lactante zarandeado y osteogénesis imperfecta

Shaken baby syndrome (SBS) is a form of physical abuse that includes the presence of a subdural or subarachnoid haematoma or diffuse cerebral oedema, retinal haemorrhages and, in general, absence of other physical signs of traumatic injury. Osteogenesis imperfecta (OI) is a genetic disorder affecting the synthesis of type I collagen that leads to brittle bones with frequently occurring fractures, with presenting clinical symptoms taking a variety of forms. A differential diagnosis allowing it to be distinguished from physical abuse is known, due to the existence of bone fractures with no known traumatic injuries, but we do not understand the link between OI and SBS. We describe the case of an infant who, at the age of 3 months, suffered symptoms of acute encephalopathy with convulsions, subdural haematoma and retinal haemorrhages compatible with SBS, as well as bilateral rib fractures. The skeletal series of X-rays revealed alterations in bone structure and texture, which led to a diagnosis of OI that was confirmed by a study of the collagen in skin fibroblasts. The suspected existence of SBS is unpleasant both for the health care professional and for the patient's relatives. The existence of rib fractures in an obvious case of shaken baby syndrome suggested malicious abuse; however, the parents' attitude and the existence of OI made us think that no harm was intended. Shaking could have been secondary to bouts of crying due to microfissures related to the OI. The differential diagnosis of processes that can be mistaken for shaken baby or from favourable or predisposing medical factors must be taken into consideration.

Encephalopathy After Bone Marrow Transplantation

Encephalopathy After Bone Marrow Transplantation

Posttraumatic Intracerebral Venous Thrombosis: An Infant Who Has Fallen Off a Hammock

A 45-day-old boy presented with drowsiness, pallor, and respiratory failure of about 24 hours' duration. Initially, the family gave no history of trauma, but after the laboratory investigations, they admitted that he had fallen off a hammock. On the plain films and cranial computed tomography (CT), no fracture of the cranium was detected, but cranial CT and magnetic resonance imaging revealed thrombosis in the sigmoid sinus, superior sagittal sinus, and straight sinus; right subdural hematoma; diffuse cerebral edema; and diffuse infarction in the right posterior temporal, parietal, and occipital lobes. Full recovery was achieved by anticoagulation with unfractionated heparin within 14 days. Falling off a hammock was the only risk factor for this patient. Thus, when cerebral thrombosis develops in childhood, trauma should be considered regardless of whether such information is provided by the family.

Status epilepticus after a massive intravenous N-acetylcysteine overdose leading to intracranial hypertension and death

Cases of N-acetylcysteine overdose have been reported before. In some cases, these overdoses have led to death if an anaphylactoid reaction was present. A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.

A proposed treatment modality for contrast-induced encephalopathy

Background: Angiography is a relatively common procedure with a low rate of complications. One of the most difficult complications encountered is that of contrast-induced encephalopathy. Unfortunately, there still is no standard treatment available for this. We studied a series of patients with contrast-induced encephalopathy immediately following angiography. Methods: A total of 3 patients were studied. Each patient had just undergone angiography. A deterioration in neurological status following this procedure prompted further work-up. A CT scan and/or an MRI of the brain was performed. One patient underwent a craniectomy while the others did not. Their clinical course was observed and documented. Results: The patient who underwent craniectomy had a better outcome as compared to those without surgical intervention, in terms of quality of life, and survival. Conclusion: The imaging studies supporting contrast-induced encephalopathy consistently demonstrated a pattern of diffuse cerebral edema, with retention of contrast material. In previous studies, no interventions for diffuse edema caused by contrast agents were suggested. From this series, we propose that craniectomy is a beneficial procedure. The rationale for this recommendation is that this would allow more room for the expanding brain parenchyma.

Recombinant activated factor VII for the rapid correction of coagulopathy in nonhemophilic neurosurgical patients.

Coagulopathy is a significant contraindication for neurosurgery. Unfortunately, many coagulopathic patients require urgent neurosurgical intervention. Standard use of blood products, including fresh-frozen plasma or prothrombin complexes, to correct the coagulopathy often leads to significant delays in treatment. Recombinant activated factor VII (rFVIIa) is a medication originally designed to treat bleeding in hemophiliacs but also seems to correct a wide variety of coagulopathies rapidly and safely in nonhemophilic patients. The medical records of nine patients with coagulopathy requiring urgent neurosurgical intervention were reviewed retrospectively. Each patient was given a dose ranging from 40 to 90 microg/kg of rFVIIa before undergoing surgery. Pre-rFVIIa coagulation and post-rFVIIa coagulation parameters were obtained. Once correction of the coagulopathy was verified, each patient underwent the appropriate neurosurgical procedure. The average age of the patients was 40.9 years; six were women. The causes of the coagulopathy included anticoagulant medication, liver dysfunction, and dilutional coagulopathy after traumatic hemorrhage. Neurosurgical indications included intraparenchymal/intraventricular hemorrhage, hydrocephalus, diffuse cerebral edema, and epidural hematoma. Post-rFVIIa coagulation parameters obtained as early as 20 minutes after infusion of the medication showed normalization of values. There were no procedural or operative complications and no postoperative hemorrhagic complications. No associated thromboembolic or other complications with the use of rFVIIa were observed. The use of rFVIIa for the urgent surgical treatment of coagulopathic patients is quite promising. Further studies, including randomized, prospective trials using rFVIIa to address issues such as optimal dosing, efficacy, surgical indications, cost-effectiveness, morbidity, and mortality are needed.

Adult cerebral malaria: prognostic importance of imaging findings and correlation with postmortem findings.

To correlate imaging abnormalities, clinical features, and postmortem findings in patients with proved cerebral malaria. Twenty-one patients aged 17-50 years with cerebral malaria consented to undergo transverse nonenhanced (10-mm sections) and contrast material-enhanced (8-mm sections in posterior fossa and 10-mm sections in supratentorial region) CT on admission (n = 21) and on day 10 (n = 6), with thin sections (5 mm) obtained in the area of abnormality. All CT scans were evaluated for diffuse cerebral edema, focal parenchymal abnormalities, and hemorrhage. CT findings were categorized as normal, diffuse cerebral edema, and edema with thalamic hypoattenuation without or with cerebellar hypoattenuation. Spearman rank correlation test was performed. Initial scans were normal in seven patients with mild disease (median Acute Physiology and Chronic Health Evaluation [APACHE] II score of 7, median Glasgow Coma Scale [GCS] score of 10), and all survived. Of eight patients with diffuse cerebral edema (GCS > or = 8; median APACHE II, 21), six survived. Cerebral edema with thalamic and cerebellar white matter hypoattenuation was seen in five patients. All had GCS score of 6 or less, median APACHE II score of 26, and multiorgan failure; none survived. One patient (GCS = 6) had thalamic hypoattenuation without cerebellar lesions. He survived with mild residual hemiparesis. Diffuse petechial hemorrhages were seen in the cerebrum and cerebellum at autopsy in all seven patients who died. These petechial hemorrhages were not visualized on CT scans. CT findings did not correlate with degree of parasitemia. CT findings correlate well with level of consciousness and severity of disease but underestimate the extent of disease at pathologic examination. A normal CT scan indicates a favorable outcome, whereas cerebellar hypoattenuation portends a poor outcome.

Decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered?

The management of refractory post-traumatic cerebral oedema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high, despite refinements in medical and pharmacological means of controlling intracranial hypertension. In this retrospective study we have evaluated the efficacy of decompressive craniectomy as a last resort therapy, from the data of nine patients with severe brain injury and delayed cerebral oedema (diffuse injury type III), treated between January 1997 and September 1999. The following parameters were considered: age, Glascow Coma Scale, injury severity, intracranial pressure, CT findings, pupil reaction/posturing. Follow-up period was over at least 2 years and outcome measured on the GOS. Patients have been operated on post-trauma median day 3, mean age 26+/-9, GCS 7+/-3.7, mean APACHE II 16+/-6.4, mean ISS 27.8+/-16.1, mean preoperative ICP 37.7+/-10.0, mean postoperative ICP 18.1+/-16.01. Seven patients have been operated by a frontotemporoparietal approach (six of them bilateral, one unilateral) and two patients have been operated on by a bilateral subtemporal approach. Mortality rates 22%, severe disability 11%, good recovery 66%. Patients with STBI, developing delayed intracranial hypertension caused by diffuse cerebral oedema, definitely benefit from craniectomy when current medical treatment has failed. The encouraging results of outcome in this and more recent studies, indicate the need for a multi-institutional randomized prospective study evaluating early indicators of raised ICP, timing, efficacy of treatment, operative technique and complications of decompressive craniectomy.

Craniectomía descompresiva en niños con traumatismo encefalocraneano grave, una alternativa terapéutica en la hipertensión endocraneana refractaria: Presentación de dos casos clínicos

Introduction : Decompressive craniectomy continues to be a controversial treatment in children with post traumatic diffuse cerebral oedema who develop severe intracranial hypertension (SIH) refractory to conventional treatment. This is because there is no agreement in its exact indications or its real efficiency. Objective : To report the results of decompressive craniectomy used in the paedriatric ICU of the Dr. Sotero del Rio Hospital in 2 patients aged 2 months and 8 years with a diagnosis of severe head injury and SIH refractory to conventional medical treatment. They presented with a Glasgow coma scale of 5, a cerebral scanner excluded lesions with a mass effect and had SIH (over 40 mmHg) and a cerebral perfusion pressure (CPP) over 60 mmHg. They were submitted to a bifrontal decompressive craniectomy to control intracranial pressure. Both patients survived; one with permanent severe sequelae and the other with minimal sequelae and an adequate social rehabilitation. Conclusions : Monitoring intracraneal pressure and image studies as part of a total neurointensive evaluation would identify those patients with a risk of uncontrolable cerebral oedema, in which decompressive craniectomy should be considered as a useful alternative treatment to prevent secondary irreversible brain damage.

Leucoencefalitis aguda hemorrágica de Weston Hurst. Estudio neuropatológico de un caso

Acute hemorrhagic leukoencephalitis (AHL), or Hurst disease is a rare, usually fatal, disease, probably due to an autoimmune cross reaction against myelin antigens present in the central nervous system, and which forms a spectrum of post infeccious demyelinating diseases with acute disseminated encephalomyelitis. The patient was a 21 year old female who presented with an acute encephalopathy and generalized seizures following a 15 day febrile syndrome attributed to amygdalitis; a laboratory work up, including CSF, was non diagnostic, and a brain CT scan revealed diffuse cerebral edema. After 12 days the patient died from nosocomial pneumonia and multi organ failure; neuropathological examination of the brain confirmed the diagnosis of Hurst acute hemorrhagic leukoencephalitis, with a weak perilesional inflammatory reaction, unlike the usual picture in AHL. AHL should be a part of the differential diagnosis of acute encephalopathic diseases, particularly if preceded by systemic infections. The atypical laboratory findings, and the impossibilty of performing a brain MRI were obstacles to the diagnosis in this case. The relative paucity of the perivascular infiltrate is an atypical finding, and could be due to apoptotic clearance of the inflammatory cells, as has been described in other autoimmune demyelinating diseases.

Degenerative Disorders of the Central Nervous System

Degenerative Disorders of the Central Nervous System

Hemochromatosis as a Risk Factor for Fulminant Staphylococcus aureus Pneumonia*

Hemochromatosis as a Risk Factor for Fulminant Staphylococcus aureus Pneumonia*

Excellent coronary perfusion pressure during cardiopulmonary resuscitation is not good enough to ensure long-term survival with good neurologic outcome: a porcine case report

Purpose: To report a case of cerebral ischemia confirmed by magnetic resonance imaging after successful cardiopulmonary resuscitation (CPR) complicated by acute respiratory injury. Materials and methods: After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, a female pig weighing 38 kg received every 5 min vasopressin (0.4, 0.4 and 0.8 U/kg). After 22 min of cardiac arrest, including 18 min of CPR, one defibrillation attempt employing 100 J resulted in return of spontaneous circulation. Neurological evaluation was performed 24 and 96 h after successful CPR. Magnetic resonance imaging was carried out 4 days after CPR using a clinical 1.5 T scanner. The magnetic resonance imaging protocol consisted of fast spinecho T2-weighted, as well as spinecho T1-weighted imaging of the brain. Results: CPR with vasopressin resulted in excellent coronary perfusion pressure ranging between 35 and 60 mmHg throughout CPR. Eight minutes after initiation of chest compressions, bleeding out of the tracheal tube occurred. This was later confirmed as originating from bilateral bloody pulmonary infiltrations, resulting in acute respiratory injury in the post-resuscitation phase. Ninety-six hours after successful CPR, magnetic resonance imaging revealed bilateral diffuse cerebral vasogenic edema. Conclusion: Although excellent coronary perfusion pressure renders a return of spontaneous circulation more likely, complications such as acute respiratory injury in the post-resuscitation phase have to be managed carefully in order to ensure good neurological recovery from cardiac arrest.

Acute pit gas (hydrogen sulfide) poisoning in confinement cattle.

Rapid deaths in confinement cattle caused by exposure to hydrogen sulfide (H2S) gas from manure pits has not been reported in the USA. In 1997, 158 cattle in 2 confinement pens were exposed to H2S gas as the manure in the pits under a slatted floor was agitated prior to pumping. Approximately 35 of the cattle were lying on the floor when the upper agitator was turned on. Within 5 minutes, many these cattle were down on their sides and paddling. Of these, 26 died within a few minutes. The survivors were treated and sent to slaughter. Cattle that did not show immediate signs of toxicosis remained clinically unaffected. Two steers that were near death were brought to the Purdue Animal Disease Diagnostic Laboratory for clinical evaluation, euthanasia, and necropsy. They were recumbent and unresponsive to visual and auditory stimuli. Necropsy examination yielded no significant gross lesions. No evidence of viral or bacterial infection was found. Ocular fluid nitrate concentrations were within normal limits, and no lead was detected in either animal. Microscopic examination revealed lesions consistent with H2S-induced central nervous system anoxia. Histologically, sections of brain demonstrated massive, diffuse cerebral cortical laminar necrosis and edema. Portions of the outer lamina contained hypereosinophilic and shrunken neurons. The subcortical white matter was vacuolated in some areas. The history, clinical signs, and histologic lesion of cerebral laminar necrosis led to a diagnosis of H2S toxicosis in these cattle.

Fatal Hydrocephalus in a Patient with Neurofibromatosis

Associate ProfessorAssistant ProfessorResidentDepartment of AnesthesiologyUniversity of Texas Health Science CenterHouston, Texas, 77030epivaliz@anes1.med.uth.tmc.eduTo the Editor:—Anesthetic implications of neurofibromatosis may include airway, mediastinal and vertebral neurofibromas, associated endocrine syndromes, and intracranial masses in 5–10% of patients. 1Hydrocephalus is a rare manifestation of neurofibromatosis and is commonly described during the first two decades of life. 2–4We present a case of acute postoperative hydrocephalus in a previously healthy 21-yr-old patient with neurofibromatosis.The patient presented for excision with bilateral flap closure of a 12-cm cutaneous neurofibroma of the posterior neck and back. He had another neurofibroma on a toe, cafe-au-lait spots, and no history of seizures or intracranial disease and was otherwise in good health. The 4-h anesthesia and surgery was uneventful, with careful prone positioning, and the patient was discharged, awake, from the recovery room. Over the next 6 h, the patient received hydrocodone (two tablets), promethazine (12.5 mg), morphine (4 mg), and promethazine (12.5 mg). One hour after the morphine–promethazine (12 h after surgery), the patient’s mother reported that the patient had a headache, had vomited, and may have had a seizure. At assessment, the patient was found to be unresponsive and was immediately intubated and resuscitated by an anesthesiologist who was on the floor at the time. Pupils were fixed and dilated, computed tomography showed severe obstructive hydrocephalus with transtentorial herniation, severe diffuse cerebral edema, and an ill-defined area of decreased density in the right thalamus. Although a ventriculostomy was placed, the patient remained unresponsive and was declared brain dead the following day.The computed tomography findings were compatible with a diagnosis of aqueduct stenosis, and the cause of the acute increase in intracranial pressure was speculated to have resulted from a seizure. In retrospect, the presumed nausea, necessitating perphenazine 1 h before arrest, may have heralded an increase in intracranial pressure.We present this case to alert anesthesiologists to the rare and potentially life-threatening association of obstructive hydrocephalus in patients with neurofibromatosis. The absence of symptoms does not preclude the diagnosis with late presentation described, and preoperative assessment should include a search for previous cranial imaging. If not available, as in this case, imaging should be considered before elective surgery in light of recommendations for routine imaging in these patients. 4

Rehabilitation outcome following traumatic brain injury--the Singapore experience.

The objectives of this study were to define (1) demographic and injury characteristics for acute traumatic brain injury (TBI) patients admitted to rehabilitation; (2) admission and discharge functional status; (3) discharge disposition and vocation status at follow-up. The charts of 80 consecutive TBI admissions (64 males, 16 females) were reviewed. Outcome measures included admission and discharge Modified Barthel Index (MBI) scores, length of rehabilitation stay, discharge disposition and return-to-work status at 1 year post-injury. Fifty-seven (71.3%) of patients were aged 40 years or less. Motor vehicle accidents accounted for 70.0% (56) of injuries. Sixty-one (76.3%) had severe head injuries. Diffuse cerebral oedema was present in 41.3% (33) and 52.5% (42) had intracranial haematoma. Admission and discharge MBI scores were 49.6 +/- 33.7 and 76.9 +/- 25.6 respectively. This difference was significant (P < 0.001). Memory and planning/organization deficits were present in 68.6% and 70.5% of patients (51 tested). Multiple regression analysis showed that admission MBI score had significant influence on discharge functional outcome (Multiple R 0.66, R2 0.40, P < 0.001). Seventy-two (90%) were discharge home and 25% (20) returned to work at 1 year post-injury. We conclude that this cohort of TBI patients showed significant improvement in functional status after rehabilitation, and admission functional status had the most impact on discharge functional outcome.

Nickel.

Nickel is an essential element for at least several animal species. These animal studies associate nickel deprivation with depressed growth, reduced reproductive rates, and alterations of serum lipids and glucose. Although there is substantial evidence of an essential status for nickel in animals, a deficiency state in humans has not been clearly defined. Nickel is a silver-white metal with siderophilic properties that facilitate the formation of nickel-iron alloys. In contrast to the soluble nickel salts (chloride, nitrate, sulfate), metallic nickel, nickel sulfides, and nickel oxides are poorly water-soluble. Nickel carbonyl is a volatile liquid at room temperature that decomposes rapidly into carbon monoxide and nickel. Drinking water and food are the main sources of exposure for the general population with the average American diet containing about 300 micrograms Ni/d. Nickel is highly mobile in soil, particularly in acid soils. There is little evidence that nickel compounds accumulate in the food chain. Nickel is not a cumulative toxin in animals or in humans. Almost all cases of acute nickel toxicity result from exposure to nickel carbonyl. The initial effects involve irritation of the respiratory tract and nonspecific symptoms. Patients with severe poisoning develop intense pulmonary and gastrointestinal toxicity. Diffuse interstitial pneumonitis and cerebral edema are the main cause of death. Sodium diethyldithiocarbamate is an investigational drug used to chelate nickel following exposure to nickel carbonyl. Nickel is a common sensitizing agent with a high prevalence of allergic contact dermatitis. Nickel and nickel compounds are well-recognized carcinogens. However, the identity of the nickel compound or compounds, which cause the increased risk of cancer, remains unclear. Currently, there are little epidemiological data to indicate that exposure to metallic nickel increases the risk of cancer, or that exposure to the carcinogenic forms of nickel causes cancer outside the lung and the nasal cavity.

The pseudo-delta sign is unreliable in differentiating between aneurysmal SAH and sinus thrombosis in unenhanced brain CT

The pseudo-delta sign (PDS) consists of a hyperdense extra-axial triangular image surrounding the low density of the superior sagittal sinus (SSS) in the unenhanced brain CT scan (Fig. 1) [1]. The true delta or empty-delta sign, described by Buonanno et al. in 1978, is only visible on contrast-enhanced films (Fig. 2) [1–4]. The PDS has been described in association with interhemispheric subdural hemorrhage, subarachnoid hemorrhage (SAH) and superior sagittal sinus thrombosis (SSST) [1–5]. The sign has also been encountered with increased attenuation of normal dura surrounding the SSS, diffuse cerebral edema in children and sluggish flow resulting from raised intracranial pressure. Others include calcification of arachnoid granulations and possibly brain death [3,4,6–8]. In an autopsy study of 12 patients with ‘empty triangle sign’, another descriptive term for the PDS, Zilkha et al. found that five of of the patients had SSST. However, they noticed that this sign was not specific for SSST as it was also observed in SAH [3]. The aim of this study was to compare the frequency of PDS in our patients with SAH, SSST as well as in other neurological conditions and to infer its diagnostic accuracy.

Fractured cervical spine and aortic transection

A 17-year-old victim of a road traffic accident presented. Following investigation diagnoses of fractured first cervical vertebra, aortic transection, diffuse cerebral oedema, fractured right ribs 2-4 and pubic rami were made. Management of this case presented a number of anaesthetic dilemmas: management of the airway, use of cross-clamp vs. shunting or heparinization and bypass, cardiovascular and neurological monitoring, maintenance of cardiovascular stability during and post cross-clamp, minimizing the risk of post-operative renal and neurological dysfunction.

CT findings in neonatal hypothermia.

Newborn infants are particularly prone to hypothermia, a condition with a high mortality. To study the CT brain patterns in infants with hypothermia and neurological symptoms. We reviewed the brain CT of nine infants with neonatal hypothermia, multiple organ failure, seizures and coma. Two infants had normal CT scans, acutely and at follow-up, and were clinically normal at follow-up. In seven infants, CT showed diffuse cerebral oedema, with reversal of the normal density relationship between grey and white matter and a relative increased density of the thalami, brainstem and cerebellum - the 'reversal sign'. In six surviving infants with severe developmental delay, follow-up CT revealed cerebral atrophy with multicystic encephalomalacia. The 'reversal sign' has been described in the abused child, birth asphyxia and anoxia due to drowning. Neonatal hypothermia is offered as a further cause.