Apparently healthy children living in areas where rickets is prevalent have risk factors for rickets and a small proportion will have evidence of biochemical rickets.

A prospective study was conducted to study the splenic function among sickle cell anemia (SCA) patients in Qatif (Eastern Province of Saudi Arabia). Seventy-seven patients (30 children and 47 adults aged 2-57 years) were included. (99m)Tc stannous colloid liver-spleen scan was done for each patient during steady state. The splenic function was graded from 0 to 4 in relation to liver uptake. Seventy percent of our patients showed evidence of splenic hypofunction, and most of them (83%) had severe hyposplenism. Up to the age of 4 years, only 17% of the children showed evidence of functional hyposplenism, but by the age of 10 years >50% were hyposplenic. Most of the hyposplenic children had functional hyposplenism, whereas only one-third of hyposplenic adults had autosplenectomy. There was no effect of level of HbF on the frequency of hyposplenism, but on the other hand low MCV seems to be protective against hyposplenism. A significant number of adult SCA patients have clinically enlarged spleens, and almost a third have normally functioning spleens. Because of the low prevalence of hyposplenism in children younger than 4 years of age, routine penicillin prophylaxis is probably not indicated in this population, an issue which needs further evaluation.

A 16-month old Saudi boy was admitted to the Emergency Room (ER) of King Faisal University Hospital; he was drowsy and extremely ataxic and was vomiting. The mother noticed that the child had progressive unsteady gait and was crying from headaches and vomiting for a month prior to his admission to this hospital.On admission, he was found to have marked bilateral papilloedema. The right pupil was slightly more dilated than the left. Both pupils showed sluggish reaction to light. Responses were extensor bilaterally. Emergency CT scan showed an enhancing mass compressing the cerebellum from the right side. The scan did not reveal evidence of tumour elsewhere intracranially. The fourth ventricle was distorted with associated hydrocephalus (Fig. 1 A).Emergency operation was performed on August 3, 1989 for seemingly total removal of a posterior fossa malignant tumour, through suboccipital craniectomy and atlas laminectomy. At operation, the tumour was very adherent to the dura; the dura was dissected. The tumour was dark greyish brown in colour, relatively vascular and unencapsulated. There was a clear line of cleavage between the tumour and the compressed cerebellum. External drainage was left in the lateral ventricle through a separate burr hole. The patient showed marked improvement. Nine days later, VA shunt was inserted. As the patient developed meningitis and ventriculitis, a few days later, the shunt was replaced by external drainage. The patient's condition deteriorated and he became unconscious. He was responding to pain stimuli by flexion withdrawal. He had cardiac arrest twice during two weeks.After the infection subsided, bilateral ventricular shunts were inserted. On 12.9.1989, he became unable to breath and was bradycardic. CT scan showed a large recurrence of the tumour. At an emergency operation done then, the tumour was found infiltrating the cerebellum, vermis, and the brain stem. Only partial removal was possible because of the infiltration of the tumour into the brain stem. A follow-up CT scan done 10 days later showed reduction in the size of the tumour. Two weeks later, the patient was decerebrate, unable to breath, and hypothermic. CT scan revealed a huge growth of the tumour, supra and infratentorially (Fig. 1 B). The patient died on 26.10.1989. Autopsy unfortunately was not permitted. Pathological Features."The tumour is composed of atypical bizarre cells, with large hyperchromatic granular nuclei and prominent nucleoli encore-

of the Annals of Saudi Medicine by Sharma et al [1]. While its possible development cannot be overlooked as a cause of deterioration in the course of treatment of head-injured patients, nevertheless it is worth pointing out that in some cases it could be silent despite its multiplicity and therefore, its presence does not necessarily preclude other reasons for the deterioration.We would like to draw attention to that point through this illustrative case:A 36-year-old Saudi male was brought to the emergency room after a car accident. He had sustained a head injury with a 3-inch right temporoparietal scalp laceration but no underlying skull fracture. In addition, he suffered both pelvic fracture and a left knee ligament rupture. His admission Glasgow Coma Scale (GSC) score was 10/15 and he had a focal left hemiparesis. His initial computerized tomographic (CT) scan was almost normal except for his mild right hemispheric contusion. After resuscitation and stabilization (left knee immobilized in above-knee plaster and suture of the scalp laceration) he was ventilated in the intensive care unit. Forty-eight hours later his PO 2 dropped from 101 mm Hg to 63 on consistent CMV at a rate of 15/m, a tidal volume of 700 and FIO 2 of 35%. His PO 2 improved partially on increasing the oxygen flow, tidal volume and respiratory rate. Positive end-expiratory pressure (PEEP) of 5 had to be added to attain acceptable values of his PO 2 . His clinical picture was consistent with an acute respiratory distress syndrome (ARDS) which was later controlled. A follow-up scan after the institution of the PEEP clearly showed the development of two areas of delayed intracerebral hematoma in both the right frontal and left temporal lobes. The patient responded well to conservative treatment and he was extubated after fully recovering his level of consciousness. Over the subsequent week his left hemiparesis resolved, however, he had a transient episode of post-traumatic psychosis which responded well to haloperidol. The second follow-up CT scan of the brain showed the total resolution of the delayed intracerebral hematomas.In an earlier study on our head-injured patients there was a less than favorable expected outcome in patients with an initial GSC score of seven or less, particularly so in those who had a combination of acute intracerebral and subdural hematomas (78% died) [2]. The importance of follow-up CT scan in head-injured patients cannot be overemphasized, particularly so with evidence of deterioration during the course of treatment. The reported incidence of 1.5% and 7% [3,4] relates to those delayed intracerebral hematoma which become evident clinically, however, the incidence of the silent ones could conceivably be higher than those quoted. It is worth pointing out that the deterioration in our patient was likely due to the development of ARDS which preceeded the onset of the delayed intracerebral hematomas. A factor which may have hastened its formation is the use of PEEP which may well be an additional factor in the pathogenesi...

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