post-traumatic stress disorder/edema

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Post-traumatic edema: pathomechanism, diagnosis and treatment.

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Due to the unknown etiology, which prevents treatment of the causes, chronic post-traumatic edema of the lower limbs is a major clinical problem. The present article discusses the etiological factors that produce chronic post-traumatic edema, including traumatic and iatrogenic damage to lymph

Intraventricular albumin: an optional agent in experimental post-traumatic brain edema.

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OBJECTIVE Human albumin may be effective in the treatment of posttraumatic brain edema due to its hyperoncotic features. Therefore, the aim of the experimental study presented in this paper has two points: the first is to evaluate the efficacy of intraventricular hyperoncotic human albumin on

Meclofenamate sodium in the treatment of post-traumatic edema. Report of a controlled double-blind study.

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130 patients with edema as the sequel of a traumatic incident were selected for this study, 43 patients were treated with 300 mg N-(2,6-dichloro-m-tolyl)anthranilic acid, sodium salt (meclofenamate sodium, Meclomen) per day for one week, 44 patients received 600 mg oxyphenbutazone per day and 43

The use of Hypertonic Saline in the Treatment of Post-Traumatic Cerebral Edema: A Review.

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Effective methods for treating cerebral edema have recently become a matter of both extensive research and significant debate within the neurosurgery and trauma surgery communities. The pathophysiologic progression and outcome of different forms of cerebral edema associated with traumatic brain

Edema and lower leg perfusion in patients with post-traumatic dysfunction.

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Impedancegraphy and laser Doppler flowmetry were used to measure whether limb circulation changes following post-traumatic immobilization and edema. Intermittent pneumatic compression was used for edema treatment. Limb blood flow due to edema was unchanged compared to the contralateral healthy leg.

[Intermittent impulse compression. An alternative in therapy of post-traumatic and postoperative edema].

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In patients with foot and ankle trauma, surgery and postoperative mobilization are often delayed because of swelling. The aim of this study was to assess if intermittent impulse compression of the foot is better than the standard therapy of applying cool packs at intervals. For intermittent impulse

RE-EXPANSION PULMONARY EDEMA FOLLOWING REPAIR OF MISSED POST TRAUMATIC DIAPHRAGMATIC HERNIA A CASE REPORT AND REVIEW OF LITERATURES.

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Reexpansion pulmonary edema following repair of missed diaphragmatic hernia is very rare .Here reported is a case of bilateral reexpansion pulmonary edema occurring after reconstruction of left sided post traumatic diaphragmatic hernia. The patient was re intubated and ventilated later put on

Erythropoietin protects from post-traumatic edema in the rat brain.

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Erythropoietin (Epo) is gaining interest in various neurological insults as a possible neuroprotective agent. We determined the effects of recombinant human Epo (rhEpo, 5000 IU per kg bw) on brain edema induced in rats by traumatic brain injury (TBI; impact-acceleration model; rhEpo administration

Norepinephrine and traumatic brain injury: a possible role in post-traumatic edema.

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Unilateral cerebral contusion is associated with an early (30 min) increase in norepinephrine (NE) turnover followed by a later (6-24 h) depression of turnover which is bilateral and widespread throughout the brain. Blockade of NE function during the first few hours after traumatic brain injury

Enoxaparin ameliorates post-traumatic brain injury edema and neurologic recovery, reducing cerebral leukocyte endothelial interactions and vessel permeability in vivo.

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BACKGROUND Traumatic brain injury (TBI) confers a high risk of venous thrombosis, but early prevention with heparinoids is often withheld, fearing cerebral hematoma expansion. Yet, studies have shown heparinoids not only to be safe but also to limit brain edema and contusion size after TBI. Human

[Current alternative therapy of post-traumatic brain edema].

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Mortality is high among patients developing post-traumatic brain oedema and increased intracranial pressure following severe head injury. Although routine treatment varies from one centre to another it often includes one or more of such measures as hyperventilation, high-dose barbiturate therapy,

[Post-traumatic lymphatic and venous drainage changes in persistent edema of lower extremities].

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Mechanical injury of soft tissues and bones of the lower extremity is followed by chronic edema at the site of trauma and distally to it. This complication affects almost every patient with a fracture of the lower limb. The question is whether posttraumatic edema is due to lymphatic obstruction,

[Drug modification of post-traumatic edema of the extremities by the proteinase inhibitor aprotinin. An animal experiment study].

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Posttraumatic edema remains a serious problem in traumatology. Unrecognized or improperly treated, edema poses a threat to the survival of any extremity, particularly the hand, where a number of intricate functional structures are at stake. This study, as well as other recent clinical and

[Post-traumatic edema as a limiting factor in early functional treatment measures and its pharmacodynamic modification].

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Post-traumatic oedema is a limiting factor of early functional exercise following fractures. A review of drug prophylaxis used in many clinical studies is given. A 30% reduction of oedema development following bimalleolar fractures was achieved with cyclooxigenase inhibitors (azapropazone) and

The effect of human corticotrophin releasing factor on the formation of post-traumatic cerebral edema.

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Controlled cortical impact is a well validated model of cortical contusion which is known to produce cerebral edema. Corticotrophin Releasing Factor (CRF) is a hypothalamic neuropeptide, which is known to inhibit transendothelial leakage of plasma derived fluid and tissue edema in response to

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