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Biomedical subjects

S M Peerdeman

Publications and source records attributed to S M Peerdeman.

9 recordsLinked to original sources
PubMed2006

Acquired encephaloceles and epilepsy in osteopetrosis.

Osteopetrosis is a condition in which there is a defect in bone resorption by osteoclasts. With thickening of the skull and skull base, the cranial capacity becomes compromised and skull foramina gradually occlude, resulting in a wide range of neurological symptoms and signs. We present a case of autosomal dominant osteopetrosis with temporal lobe epilepsy and nasal obstruction due to acquired bifrontal encephaloceles associated with a decreased intracranial capacity. Neurosurgical reconstruction of the frontal skull base alleviated the symptoms of epilepsy and nasal obstruction.

Adult↗
PubMed2005

Cerebral microdialysis and positron emission tomography after surgery for aneurysmal subarachnoid hemorrhage in grade I patients.

BACKGROUND: Using cerebral microdialysis, baseline values for energy-related chemical markers have been reported in awake patients. Radionuclide studies have demonstrated a locally decreased metabolism, thought to be the result of brain retraction. These baseline values, however, may not be applicable to patients after surgical aneurysm repair following a subarachnoid hemorrhage (SAH). We assessed metabolic chemical marker levels in World Federation of Neurological Surgeons Committee (WFNS) grade I SAH patients after aneurysm surgery and compared them with previously reported baseline values. METHODS: In 5 WFNS grade I SAH patients, energy-related chemical marker levels were obtained using microdialysis in the area of brain retraction after aneurysm surgery. In addition, an [(18)F]2-deoxy-d-glucose positron emission tomography (FDG-PET) was performed. RESULTS: The FDG-PET showed a decrease of glucose metabolism in the frontotemporal area. Comparing the mean values for chemical markers of this study with reported baseline values, the most striking difference was a mild decrease of pyruvate and an increase of the lactate/pyruvate ratio. In individual patients, some markers indicated possible ischemia. A consistent pattern or ischemic profile for all markers, however, was not found. CONCLUSION: FDG-PET scanning confirmed postoperative metabolic changes found in previous studies. Mean interstitial chemical marker levels ranged from normal to mildly deviant compared with reference chemical marker levels for awake patients and are likely to be applicable in SAH patients after aneurysm repair.

Adult↗
PubMed2004

Metastatic adenocarcinoma in the cerebellopontine angle, presenting as a meningioma: a case report of rare occurrence.

We present the case of a 36-year old woman who was referred to our hospital with an 8 weeks history of walking difficulties, nausea and vomiting, diminished hearing on the right side and diplopia. On Magnetic Resonance-Imaging (MRI) a tumour in the right cerebellopontine angle (CPA) was diagnosed. The tumour was resected and histopathological examination revealed an adenocarcinoma, suspicious for a metastasis from carcinoma of the breast considering the aspect of the cells, immunochemical profile, age and gender of the patient. No primary tumour was found. In cases without histopathological diagnosis, radiosurgery should be withheld when there is doubt about the clinical or radiological diagnosis.

Adenocarcinoma↗
PubMed2003

[Neuromonitoring of patients following severe brain trauma].

To a considerable extent, the neurological outcome of patients with severe brain trauma is determined by the primary injury caused by the accident. Substantial progress has been made in our understanding of the pathophysiological processes resulting in secondary brain damage after brain trauma, partly as a result of the introduction of advanced techniques of neuromonitoring. Early recognition and treatment of the symptoms leading to this type of brain damage seems crucial to the effort to improve the neurological outcome in these patients. Useful modern neuromonitoring techniques include: measurement of the intracranial and cerebral perfusion pressure and continuous electroencephalography. Methods that are also reliable and readily applicable, but less relevant clinically, include cerebral microdialysis of fluid from the extracellular space, determination of the parenchymal oxygen tension, and determination of the venous oxygen saturation. Other techniques that are not clinically applicable include: determination of the cerebral blood flow, the cortical tissue perfusion or the regional cerebral oxygenation.

Brain Damage, Chronic↗
PubMed2001

Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury.

OBJECT: Induced hypothermia in patients with severe head injury may prevent additional brain injury and improve outcome. However, this treatment is associated with severe side effects, including life-threatening cardiac tachyarrhythmias. The authors hypothesized that these arrhythmias might be caused by electrolyte disorders and therefore studied the effects of induced hypothermia on urine production and electrolyte levels in patients with severe head injury. METHODS: Urine production, urine electrolyte excretion, and plasma levels of Mg, phosphate, K, Ca, and Na were measured in 41 patients with severe head injury. Twenty-one patients (Group I, study group) were treated using induced hypothermia and pentobarbital administration, and 20 patients (Group 2, controls) were treated with pentobarbital administration alone. In Group 1, Mg levels decreased from 0.98+/-0.15 to 0.58+/-0.13 mmol/L (mean +/- standard deviation; p < 0.01), phosphate levels from 1.09+/-0.19 to 0.51+/-0.18 mmol/L (p < 0.01), Ca levels from 2.13+/-0.25 to 1.94+/-0.14 mmol/L (p < 0.01), and K levels from 4.2+/-0.59 to 3.6+/-0.7 mmol/L (p < 0.01) during the first 6 hours of cooling. Electrolyte levels in the control Group 2 remained unchanged. Electrolyte depletion in Group I occurred despite the fact that moderate and, in some cases, substantial doses of electrolyte supplementation were given to many patients, and supplementation doses were often increased during the cooling period. Average urine production increased during the cooling period, from 219+/-70 to 485+/-209 ml/hour. When the targeted core temperature of 32 micro C was reached, urine production returned to levels that approximated precooling levels (241+/-102 ml/hour). Electrolyte levels rose in response to high-dose supplementation. In the control group, urine production and electrolyte excretion remained unchanged throughout the study period. CONCLUSIONS: Induced hypothermia is associated with severe electrolyte depletion, which is at least partly due to increased urinary excretion through hypothermia-induced polyuria. This may be the mechanism through which induced hypothermia can lead to arrhythmias. When using this promising new treatment in patients with severe head injury, stroke, or postanoxic coma following cardiopulmonary resuscitation, prophylactic electrolyte supplementation should be considered and electrolyte levels should be monitored frequently.

Adolescent↗
PubMed2001

Hypothermia.

Explore the source record for details and available documents.

Cerebrovascular Circulation↗
PubMed2000

Hypomagnesemia and hypophosphatemia at admission in patients with severe head injury.

OBJECTIVE: Low serum levels of electrolytes such as magnesium (Mg), potassium (K), calcium (Ca), and phosphate (P) can lead to a number of clinical problems in intensive care unit (ICU) patients, including hypertension, coronary vasoconstriction, disturbances in heart rhythm, and muscle weakness. Loss of these electrolytes can be caused, among other things, by increased urinary excretion. Cerebral injury can lead to polyuresis through a variety of mechanisms. We hypothesized that patients with cranial trauma might be at risk for electrolyte loss through increased diuresis. The objective of this study was to assess levels of Mg, P, and K at admission in patients with severe head injury. DESIGN: We measured plasma levels of Mg, P, K, Ca, and sodium at admission in 18 consecutive patients with severe head injury admitted to our ICU (group 1). As controls, we used 19 trauma patients with two or more bone fractures but no significant cranial trauma (group 2). SETTING: University teaching hospital. PATIENTS: Eighteen patients with severe head injury admitted to our surgical ICU (group 1) and 19 controls (trauma patients with no significant cranial trauma; group 2). MAIN RESULTS: Electrolyte levels at admission (group 1 vs. group 2; mean +/- SD, units: mmol/L) were as follows. Mg, 0.57 +/- 0.17 (range, 0.24-0.85) vs. 0.88 +/- 0.21 (range, 0.66-1.42 mmol/L; p < .01). P, 0.56 +/- 0.15 (range, 0.20-0.92) vs. 1.11 +/- 0.15 (range, 0.88-1.44 mmol/L; p < .01). K, 3.54 +/- 0.59 (range, 2.4-4.8) vs. 4.07 +/- 0.45 (range, 3.6-4.8 mmol/L; p < .02). Ca, 2.02 +/- 0.24 (range, 1.45-2.51) vs. 2.14 +/- 0.20 (range, 1.88-2.46; p = NS). In group 1, 12/18 patients had Mg levels <0.70 mmol/L vs. 2/19 patients in group 2 (p < .01); in group 1, 11/18 patients had P levels below 0.60 mmol vs. 0/19 patients in group 2 (p < .01). Moderate hypokalemia (K levels, <3.6 mmol/L) was present in 8/18 patients in group 1 vs. 1/19 patients in group 2 (p < .01). Severe hypokalemia (K levels, < or =3.0) was present in 4/18 patients in group 1 vs. 0/19 patients in group 2 (p < .05). CONCLUSION: We conclude that patients with severe head injury are at high risk for the development of hypomagnesemia, hypophosphatemia, and hypokalemia. One of the causes of low electrolyte levels in these patients may be an increase in the urinary loss of various electrolytes caused by neurologic trauma. Mannitol administration may be a contributing factor. Intensivists should be aware of this potential problem. If necessary, adequate supplementation of Mg, P, K, and Ca should be initiated promptly.

APACHE↗