Scandinavian Journal of Infectious Diseases, 2014; 46: 475–477
LETTER TO THE EDITOR
Hydrocephalus in tuberculous meningitis—How fast does it develop?
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
KHUSHNUMA MULLANFIROZE & IRA SHAH From the Pediatric TB Clinic, B.J. Wadia Hospital for Children, Mumbai, India
To the Editor, A 3.5-y-old female child presented on 29 November 2012 with swelling of the left knee joint of 3-month duration, fever of 1-month duration, and 1 episode of generalized tonic–clonic convulsion 1 week prior to presentation. The left knee swelling was progressively increasing in size and causing restriction of movement. There was also irritability with loss of weight and loss of appetite. There was no history of contact with a tuberculosis (TB) patient. She was investigated by a physician. The erythrocyte sedimentation rate (ESR) was 55 mm at the end of 1 h and a Mantoux test showed an induration of 10 mm. She had been started on first-line anti-TB treatment (ATT) consisting of isoniazid (H) and rifampicin (R) along with valproic acid 7 days prior to presentation. On examination at presentation, she had pallor, rickets, generalized lymphadenopathy, and hepatosplenomegaly. Her left knee was swollen, tender, and had restriction of movement. A BCG scar was present. Signs of meningeal irritation in the form of neck stiffness and positive Kernig’s sign were noticed. Deep tendon reflexes were brisk in all four limbs, with well sustained clonus bilaterally. There was no focal neurological deficit and sensorium was normal. Cerebrospinal fluid (CSF) analysis showed 66 g/dl proteins, a white blood cell count of 260 cells/mm3 (97% lymphocytes), and 59 mg/dl glucose with simultaneous blood sugar of 96 mg/dl. HIV ELISA was negative. A chest X-ray was normal. X-ray of the left knee showed a narrowed joint space and eroded epiphyseal areas. Ultrasonography of the knee showed effusion in the joint. Magnetic resonance imaging (MRI) of the knee was advised but not done due to financial constraints. The patient was shifted to 4-drug ATT consisting of isoniazid, rifampicin, ethambutol (E), and
pyrazinamide (Z), and steroids were initiated. Valproate was continued. During her hospital stay, the child had persistent fever with weight loss and worsening irritability. MRI of the brain was done on 1 December 2012, which showed multiple granulomas in both cerebral/cerebellar hemispheres and in the pons, with peri-lesional edema (Figure 1). Meningeal enhancement along the right middle cerebral artery (MCA) groove and around the brain stem was noted. There was no hydrocephalus. Drug-resistant TB was suspected in view of the non-response and so gastric lavage was sent for TB cultures, pending which second-line ATT was initiated on 11 December, which included para-aminosalicylic acid (PAS), ofloxacin, cycloserine, ethionamide, and amikacin in addition to HRZE. On the very next day, the child developed tremors with progressive worsening of sensorium and signs of raised intracranial tension (ICT) in the form of hypertension and bradycardia, in addition to decerebrate posturing. Mannitol and hypertonic saline infusions were given but there was no response. Hence, acute development of hydrocephalus was suspected. An urgent computed tomography (CT) scan was done, which was suggestive of a significantly dilated ventricular system with periventricular CSF ooze (Figure 2). The child underwent urgent ventricular peritoneal (VP) shunt surgery after which hypertension was controlled and the child started showing spontaneous eye opening again with improvement in sensorium. The striking feature in this case was the rapidity with which the gross hydrocephalus developed, i.e., in a matter 10–12 days, requiring urgent surgical intervention. Central nervous system (CNS) TB manifests itself primarily as tuberculous meningitis (TBM) and less commonly as tubercular encephalitis, intracranial
Correspondence: I. Shah, 1/B Saguna, 271/B St Francis Road, Vile Parle (W), Mumbai 400056, India. E-mail: [email protected] (Received 27 January 2014 ; accepted 31 January 2014 ) ISSN 0036-5548 print/ISSN 1651-1980 online © 2014 Informa Healthcare DOI: 10.3109/00365548.2014.896034
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
476
K. Mullanfiroze & I. Shah
Figure 1. MRI of the brain showing multiple granulomas without hydrocephalus.
tuberculoma, or a tuberculous brain abscess. The disease begins with the development of small tuberculous foci (Rich foci) in the brain, spinal cord, or meninges [1]. The Rich foci typically follow the vascular pattern and are located both in the meninges and in the brain parenchyma. After the release of tubercle bacilli from granulomatous lesions into the subarachnoid space, a dense gelatinous exudate forms; this is most florid in the interpeduncular fossa and suprasellar region. This exudate envelops arteries and cranial nerves, creating a bottleneck in the flow of CSF at the level of the tentorial opening, leading to hydrocephalus [2]. The time-line along which hydrocephalus develops is not definite. It is almost always present in
patients who have had the disease for 4 to 6 weeks [3]. In a study from South Africa, on follow-up brain CT after 1 week in children with TBM, 8 of 29 patients (who were not shunted) developed new hydrocephalus, which led the authors to conclude that follow-up CT should be done in patients with suspected TBM within a week of the initial CT [4]. Similarly in our patient, clinically significant hydrocephalus causing raised ICT developed in 10 days. The rapidity with which hydrocephalus develops has a bearing on daily clinical practice, as early detection and prompt treatment with ventricular shunting can significantly alter the prognosis of the child.
Figure 2. CT of the brain showing periventricular ooze and hydrocephalus.
Hydrocephalus in tuberculous meningitis Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
[1] Rom WN, Garay SM. Tuberculosis. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004.
477
[2] Rich AR, McCordock HA. The pathogenesis of tuberculous meningitis. Bull Johns Hopkins Hosp 1933;52:5–37. [3] Tandon PN. Tuberculous meningitis (cranial and spinal). In: Vinken PJ, Bruyn GW, editors. Handbook of clinical neurology. Infections of the nervous system. Vol. 33. Amsterdam: North-Holland Publishing; 1978 pp 195–262. [4] Andronikou S, Wieselthaler N, Smith B, Douis H, Fieggen AG, van Toorn R, Wilmshurst J. Value of early follow-up CT in paediatric tuberculous meningitis. Pediatr Radiol 2005;35: 1092–9.
LETTER TO THE EDITOR
Hydrocephalus in tuberculous meningitis—How fast does it develop?
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
KHUSHNUMA MULLANFIROZE & IRA SHAH From the Pediatric TB Clinic, B.J. Wadia Hospital for Children, Mumbai, India
To the Editor, A 3.5-y-old female child presented on 29 November 2012 with swelling of the left knee joint of 3-month duration, fever of 1-month duration, and 1 episode of generalized tonic–clonic convulsion 1 week prior to presentation. The left knee swelling was progressively increasing in size and causing restriction of movement. There was also irritability with loss of weight and loss of appetite. There was no history of contact with a tuberculosis (TB) patient. She was investigated by a physician. The erythrocyte sedimentation rate (ESR) was 55 mm at the end of 1 h and a Mantoux test showed an induration of 10 mm. She had been started on first-line anti-TB treatment (ATT) consisting of isoniazid (H) and rifampicin (R) along with valproic acid 7 days prior to presentation. On examination at presentation, she had pallor, rickets, generalized lymphadenopathy, and hepatosplenomegaly. Her left knee was swollen, tender, and had restriction of movement. A BCG scar was present. Signs of meningeal irritation in the form of neck stiffness and positive Kernig’s sign were noticed. Deep tendon reflexes were brisk in all four limbs, with well sustained clonus bilaterally. There was no focal neurological deficit and sensorium was normal. Cerebrospinal fluid (CSF) analysis showed 66 g/dl proteins, a white blood cell count of 260 cells/mm3 (97% lymphocytes), and 59 mg/dl glucose with simultaneous blood sugar of 96 mg/dl. HIV ELISA was negative. A chest X-ray was normal. X-ray of the left knee showed a narrowed joint space and eroded epiphyseal areas. Ultrasonography of the knee showed effusion in the joint. Magnetic resonance imaging (MRI) of the knee was advised but not done due to financial constraints. The patient was shifted to 4-drug ATT consisting of isoniazid, rifampicin, ethambutol (E), and
pyrazinamide (Z), and steroids were initiated. Valproate was continued. During her hospital stay, the child had persistent fever with weight loss and worsening irritability. MRI of the brain was done on 1 December 2012, which showed multiple granulomas in both cerebral/cerebellar hemispheres and in the pons, with peri-lesional edema (Figure 1). Meningeal enhancement along the right middle cerebral artery (MCA) groove and around the brain stem was noted. There was no hydrocephalus. Drug-resistant TB was suspected in view of the non-response and so gastric lavage was sent for TB cultures, pending which second-line ATT was initiated on 11 December, which included para-aminosalicylic acid (PAS), ofloxacin, cycloserine, ethionamide, and amikacin in addition to HRZE. On the very next day, the child developed tremors with progressive worsening of sensorium and signs of raised intracranial tension (ICT) in the form of hypertension and bradycardia, in addition to decerebrate posturing. Mannitol and hypertonic saline infusions were given but there was no response. Hence, acute development of hydrocephalus was suspected. An urgent computed tomography (CT) scan was done, which was suggestive of a significantly dilated ventricular system with periventricular CSF ooze (Figure 2). The child underwent urgent ventricular peritoneal (VP) shunt surgery after which hypertension was controlled and the child started showing spontaneous eye opening again with improvement in sensorium. The striking feature in this case was the rapidity with which the gross hydrocephalus developed, i.e., in a matter 10–12 days, requiring urgent surgical intervention. Central nervous system (CNS) TB manifests itself primarily as tuberculous meningitis (TBM) and less commonly as tubercular encephalitis, intracranial
Correspondence: I. Shah, 1/B Saguna, 271/B St Francis Road, Vile Parle (W), Mumbai 400056, India. E-mail: [email protected] (Received 27 January 2014 ; accepted 31 January 2014 ) ISSN 0036-5548 print/ISSN 1651-1980 online © 2014 Informa Healthcare DOI: 10.3109/00365548.2014.896034
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
476
K. Mullanfiroze & I. Shah
Figure 1. MRI of the brain showing multiple granulomas without hydrocephalus.
tuberculoma, or a tuberculous brain abscess. The disease begins with the development of small tuberculous foci (Rich foci) in the brain, spinal cord, or meninges [1]. The Rich foci typically follow the vascular pattern and are located both in the meninges and in the brain parenchyma. After the release of tubercle bacilli from granulomatous lesions into the subarachnoid space, a dense gelatinous exudate forms; this is most florid in the interpeduncular fossa and suprasellar region. This exudate envelops arteries and cranial nerves, creating a bottleneck in the flow of CSF at the level of the tentorial opening, leading to hydrocephalus [2]. The time-line along which hydrocephalus develops is not definite. It is almost always present in
patients who have had the disease for 4 to 6 weeks [3]. In a study from South Africa, on follow-up brain CT after 1 week in children with TBM, 8 of 29 patients (who were not shunted) developed new hydrocephalus, which led the authors to conclude that follow-up CT should be done in patients with suspected TBM within a week of the initial CT [4]. Similarly in our patient, clinically significant hydrocephalus causing raised ICT developed in 10 days. The rapidity with which hydrocephalus develops has a bearing on daily clinical practice, as early detection and prompt treatment with ventricular shunting can significantly alter the prognosis of the child.
Figure 2. CT of the brain showing periventricular ooze and hydrocephalus.
Hydrocephalus in tuberculous meningitis Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
Scand J Infect Dis Downloaded from informahealthcare.com by Florida International University on 12/28/14 For personal use only.
[1] Rom WN, Garay SM. Tuberculosis. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004.
477
[2] Rich AR, McCordock HA. The pathogenesis of tuberculous meningitis. Bull Johns Hopkins Hosp 1933;52:5–37. [3] Tandon PN. Tuberculous meningitis (cranial and spinal). In: Vinken PJ, Bruyn GW, editors. Handbook of clinical neurology. Infections of the nervous system. Vol. 33. Amsterdam: North-Holland Publishing; 1978 pp 195–262. [4] Andronikou S, Wieselthaler N, Smith B, Douis H, Fieggen AG, van Toorn R, Wilmshurst J. Value of early follow-up CT in paediatric tuberculous meningitis. Pediatr Radiol 2005;35: 1092–9.
