Perineal groove leading to a suspicion of child sexual abuse

The child’s guardian, the grandmother discovered a red ulcer in the perineum of a two years and two months old baby girl during bathing. She did not remember excessive crying or blood in the baby’s clothes in the recent past but could not confidently exclude child abuse because drunken friends of her husband used to visit their house. Medical officers suspected anal penetration with a tear extending to the vulva.


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The child's guardian, the grandmother discovered a red ulcer in the perineum of a two years and two months old baby girl during bathing.She did not remember excessive crying or blood in the baby's clothes in the recent past but could not confidently exclude child abuse because drunken friends of her husband used to visit their house.Medical officers suspected anal penetration with a tear extending to the vulva.
Examination showed a well nourished baby without any bodily injury or old traumatic scars.Genital examination revealed a triangular shaped gradual narrowing of the posterior fourchette continuing as a 2 mm wide, 5 mm deep midline red groove into the anus and up to the anterior wall of the anus.There was no contact bleeding or granulation tissue to suggest the groove was a result of injury.Base of the anterior wider triangular part of the groove was covered with the continuation of vulval mucous membrane (Figure 1 and 2).The hymen was of annular type and was intact.The hymenal orifice was about 2 mm in diameter.Anal sphincter was normal.This was a rare developmental defect known as perineal groove, a wet sulcus that extends from the posterior fourchette to the anus [1].When it presents late, medical practitioners tend to misdiagnose it for dermatological conditions [2,3].

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This congenital deformity was differentiated from an injury because of regular margins, absence of evidence of healing (granulation tissue or scarring edges), absence of other associated injuries or scars, and the distribution of the lesion exactly in the midline with equal depth throughout the course.Traumatic tears (lacerations) become shallow gradually before disappearance have irregular edges and show evidence of healing consisting of granulation tissues in a few days, scars in the edges in weeks and ultimately a complete scar.The diagnosis in this child was established because of the mucous membrane covering the lesion which was discovered when the baby was examined under anaes-thesia [4].Seven days after admission the lesion did not show any features of healing (Figure 3).The Police inquired why the congenital deformity was not discovered soon after birth.This was because the lesion was only visible when the buttocks were separated.
A 59-years old man presented with worsening chronic ataxia and recent onset dysarthria, deafness and dementia of three months.Over five years, he was investigated for unsteady gait and found bilateral cerebellar and pyramidal tract signs which were attributed to cerebellitis and transverse myelitis respectively.He already had an indwelling urinary catheter for suspected prostatism.
Ten years ago warfarin was commenced on him for a cardiac apical aneurysm and left ventricular dysfunction but recurrent haematuria and haemoptysis lead to withdrawal of it two years later.No past history suggestive of sub-arachnoid haemorrhage (SAH), head trauma or neurosurgeries were elicited.He had bilateral VIIIth nerve palsy and cerebellar signs.Spastic legs had extensor plantars but proprioception and sensorium were intact.Examination otherwise was unremarkable.Basic haema-tology, coagulation and biochemistry were normal and CT brain showed bilateral cerebellar atrophy with normal ventricles.The CSF was normal except for numerous erythrocytes.Audiogram revealed bilateral sensory neural hearing loss (SNHL) and T2W MRI brain and spinal cord showed hyposignal intensity along leptomeninges (Figures1 and 2).Patient was managed symptomatically.
Superficial cerebral hemosiderosis (SCH) is a rare disease caused by deposition of haemosiderin in superficial and sub-pial layers of CNS due to repeated chronic SAH or bleeding from CNS tumors and vascular malformations [1].A single SAH is usually insufficient to result SCH and often a clinical SAH is unapparent and source of bleeding is obscure.Anticoagulants are a known but an uncommon association [2].Classic symptom triad includes cerebellar dysfunction, SNHL and pyramidal tract signs but dementia and incontinence are common.Definitive diagnosis is by MRI, autopsy or neurosurgical findings of superficial hemosiderin deposition of CNS [3].Usually the gap between onset of symptoms and diagnosis is many years.Hypo-intensity of CNS marginal zones on T2W MRI indicates an iron induced susceptibility effect which is pathognomonic for SCH [4].Definitive treatment is by correcting the bleeding source.Iron chelators are ineffective.