Article, Psychiatry

Asymptomatic posttraumatic pneumocephalus

other related department’s consultations; the underlying diagnosis of self-mutilation should be found and necessary assistance for the patient to benefit from psychiatric treatment service should be provided. Yet, medical or surgical treatment and stabilization are urgent primary approaches in self-mutilative patients, with regard to recurrent morbidity and potential mortality, psychiatric/ psychosocial following should not be neglected; other possible self-mutilations should be prevented.

Bulent Erdur MD Ibrahim Turkcuer MD

Department of Emergency Medicine Medical Faculty, Pamukkale University Kinikli 20070, Denizli, Turkey

E-mail address: [email protected]

Hasan Herken MD

Department of Psychiatry Medical Faculty, Pamukkale University Kinikli 20070, Denizli, Turkey



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Asymptomatic posttraumatic pneumocephalus

A 22-year-old man presented to the Royal Perth Hospital ED after an alleged assault. Clinical examination showed no neurologic compromise, normal reflexes, and a Glasgow Coma Scale score of 15. Vital signs and physical examina- tion were unremarkable. The patient’s medical history

revealed no disorder and no drug or alcohol use. Routine laboratory test findings were normal. A computed tomog- raphy (CT) scan revealed a longitudinal fracture through the right petrous Temporal bone. Moreover, a significant amount of intracranial gas, distributed in a parafalcine manner, was present in the anterior aspect of both frontal lobes, the right temporal lobe, and the right cerebellum (Figs. 1 and 2). No Battle’s sign or Raccoon eyes was noted. The patient subsequently developed cerebral spinal fluid otorrhea. No neurosurgical intervention was deemed necessary, and the patient’s base of Skull fracture was treated conservatively. He was discharged from the hospital with scheduled neurologic follow-up.

The incidence of pneumocephalus is reported to be between 0.5% and 1.0% of patients with a traumatic brain injury [1]. The incidence is significantly higher in patients with basilar Skull fractures, with one study noting a 10-fold increase [2]. Studies measuring the incidence of pneumo- cephalus using CT scans report higher Incidence rates because of the enhanced sensitivity of the imaging [3]. Furthermore, the earlier after an injury that patients are imaged, regardless of technique, the more likely pneumo- cephalus is detected.

Acute traumatic pneumocephalus is diagnostic of a basilar skull fracture, whereas late pneumocephalus, which appears a few days postinjury, is suggestive of a cerebral spinal fluid fistula. Posttraumatic pneumocephalus occurs when there is a continuous, albeit sometimes very slow, collection of intracranial air. This type of pneumocephalus may produce mass effect and, as a consequence, neurologic signs/symptoms and a deterioration in functional status. Typical symptoms include increased intracranial pressure (eg, vomiting, nausea, and headache) and impaired con- sciousness. Other neurologic signs, including seizures, visual field defects, and behavioral changes, have been reported [4]. Acute complications include venous air

Fig. 1 Initial axial Brain CT scan showing a bilateral frontal pneumocephalus.

Fig. 2 Initial coronal brain CT scan showing a bilateral frontal pneumocephalus.

embolism and death from brainstem herniation. There have also been reports of cerebral infarction with subsequent development of seizure disorder from a tension pneumocele. Such morbidity stresses the need for early identification and prompt treatment [5]. It is possible to see focal findings without Elevated intracranial pressure among cases in which there is prolonged development of the posttraumatic pneumocephalus, thereby suggesting compensation for pressure changes caused by Volume expansion. Neurologic deterioration has been associated with pneumatoceles of volumes as low as 25 mL of air under tension. In the case presented here, the patient was completely asymptomatic, which highlights the compensation capacity of the human brain. Nonetheless, it is relatively uncommon that such a young patient would remain asymptomatic with this extent of pneumocephalus [6]. In this asymptomatic case, the patient was managed conservatively, with bed rest and 100% oxygen therapy to wash out nitrogen and decrease intracranial gas.

Oliver P. Gautschi MD Rene’ Zellweger MD

Department of Orthopedic and Trauma Surgery

Royal Perth Hospital Perth, Western Australia 6000, Australia E-mail address: [email protected]


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Intra-Abdominal hemorrhage due to vigorous vomiting masked by the coexistence of Mallory-Weiss syndrome

Mallory-Weiss syndrome is widely discussed since 1929. It was caused by forceful vomiting or retching usually after binge consumption of alcohol. Other reasons of vomiting include infectious gastroenteritis, Peptic ulcers, hiatal hernia, volvulus, hyperemesis of pregnancy, gallstone, cholecystitis, uremia, increase intracranial pressure, use of emetics, or various kind of intoxication. The clinical manifestations of Mallory-Weiss syndrome range from dyspepsia, abdominal pain, tarry stool passage, and hema- temesis to hypovolemic shock [1]. We report a rare case of intra-abdominal bleeding and hypovolemic shock after vigorous vomiting after bingeing, despite the simultaneous occurrence of Mallory-Weiss tear had been under control.

A 32-year-old man without any history of diabetes, hypertension, bleeding tendency, and gastrointestinal tract bleeding experienced emotional distress because of recent divorce; he consumed a large amount of wine since 7:00 pm to 10:00 pm and eventually suffered from severe Epigastric pain and vomiting. He visited the ED at about 11:18 pm that evening and reported no coffee-ground substance or bloody content in his vomitus. He denied any recent physical injuries because of trauma. Intravenous crystalloid fluid replacement and Intramuscular injection of 50 mg meper- idine were prescribed for his stabilizing his clinical condition and pain relief, respectively. Chest radiography and left decubitus view of abdominal x-ray revealed no signs of pneumoperitoneum because of hollow organ perforation. Laboratory findings included white blood cell count 8890/mL with 46.7% neutrophil, 45.3% lymphocyte, 8.0% monocyte, hemoglobin 14.9 g/dL, hematocrit 46.2%, platelet count 212 000/mL, blood glucose

148 mg/dL, creatinine 1.4 mg/dL, sodium 140 mEq/L, potassium 3.4 mEq/L, amylase 42 U/L, lipase 79 U/L, and ethanol level 133.03 mg/dL. His symptoms were improved after the supportive treatment mentioned hereinabove, and

he was discharged at about 7:00 am the other day.


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Unfortunately, because of severe epigastric pain, he revisited the ED at about 10:45 am again. This time, his vital signs were stable with body temperature at 378C, pulse rate 107 beats per minute, respiratory rate 18 times per minute, and blood pressure 135/69 mm Hg. Panendoscopy was arranged and the endoscopic findings were (1) erosive duodenitis, blub, (2) mild hemorrhagic gastritis, (3) esophageal shallow

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