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| Year : 1981 | Volume
: 27
| Issue : 3 | Page : 190-193 |
Rhinocerebral mucormycosis in a case of renal failure.
Sheth SM, Talwalkar NC, Desai AP, Acharya VN
How to cite this article:
Sheth S M, Talwalkar N C, Desai A P, Acharya V N. Rhinocerebral mucormycosis in a case of renal failure. J Postgrad Med 1981;27:190-3 |
The association of cerebral mucormycosis with various debilitating conditions like leukemia, lymphoma, carcinoma, diabetes is well known. However, there are very few case reports of mucormycosis in association with renal diseases. Besides, the treatment of such a condition also poses certain problems. The purpose of this communication is to report a case of rapidly progressing renal failure who died of cerebral mucormycosis. This paper further stresses the association between the two conditions.
Mr. V. R., a 48 year old male patient was admitted to the K.E.M. Hospital, Bombay, with a history of haematuria followed by anuria for a period over 2 days. He had developed dyspnoea and oedema over these two days. There was no other relevant renal history in the past.
On examination he was an obese individual with significant pallor. Blood pressure was 180! 100 mm of Hg. There were no phosphatic deposits in the eyes. He had cardiomegaly and tender hepatomegaly and was in congestive cardiac failure. Kidneys were not palpable. A clinical diagnosis of acute renal failure was made.
Investigations revealed urine (done later after he had 'opened up') specific gravity of 1.002. Albumin was +++. There were plenty of RBCs and granular casts were also present. Urine culture showed no growth. Blood haemoglobin was 6 gm%; PCV was 30%; Total leucocyte count was 10900/cmm. BUN was 120 mg% Serum creatinine was 9.8 mg%. Post-lunch blood sugar was 200 mg%, Serum calcium was 9.5 mg% and phosphorus was 3 mg%, Alkaline phosphatase was 2.5 KA units. Serum sodium was 130 mEq/1, potassium 6.2 mEq/1 and chlorides 92 mEq/1. Plasma bicarbonate was 15 mMol/1. In view of critical oliguria, acidosis and hyperkalemia. the patient was kept on hemodialysis. He was gradually stabilised with repeated hemodialyses. Later, after a period of 10 days he opened up and started passing some amount of urine. X-Ray KUB showed normal-sized kidneys, each measuring about 3½ vertebrae. No radio-opaque stone was seen. Drip infusion IVP failed to show any excretion and ascending pyelography did not show any obstruction. Hence a kidney biopsy was done which showed a picture suggestive of "Extra-capillary crescentric glomerulonephritis".[1] In view of this, Endoxan (2.5 mg/kg) and prednisolone (1 mg/kg.) was started. After that patient's azotemia had decreased considerably, a GTC was done which showed fasting blood sugar of 150 mg%, 1 hour-280 mg, and 2 hours 130 mg%. Hence plain insulin was started. Seven days later he started having epistaxis. No local pathology was noted by the E.N.T. surgeons. The patient did not have severe hypertension and his coagulogram was normal. He started becoming progressively drowsy over a period of the next 2 days. Diabetic coma was ruled out. He then developed periorbital oedema, chemosis of the right eye and his CNS examination revealed opthalmoplegia. There were no meningeal signs. His CSF showed 500 mg. proteins and 2090 cells out of which S5% were polymorphs. CSF sugar was 20 mg% and Chlorides were 600 mg%. A possibility of left sided brain abscess with pyogenic meningitis was thought of and the patient was put on appropriate antibiotic therapy. In view of the diabetic state with immunosuppressant treatment, fungal infection was also considered as a possibility. In view of chemosis, epistaxis and periorbital oedema, the likely fungus was thought to be mucormycosis. CSF report for fungal culture was negative. The antifungal treatment was not immediately available, hence was not started. Patient's condition continued to deteriorate and he died after 3 days.
Autopsy findings
Both the kidneys were rather small. Other organs were normal. Brain was edematous with subarachnoid haemorrhage and showed haemorrhagic infarction of the left frontal lobe. Microscopic examination of the section revealed extensive thrombophlebitis and necrosis of the tissues due to mucormycosis. The fungus was seen in the brain sections and could be grown in Saboraud's medium [Figs. 1], [Figs. 2] and [Figs. 3] On histology of the kidneys, the glomeruli showed severe degree of extracapillary cresentric glomerulonephritis.
In a patient of advanced renal failure, especially on haemodialysis, neurological deficits are not uncommon. However, with a history of fever, localising signs and abnormal CSF picture, a possibility of infective process (abscess) was more likely. In an immunologically compromised patient, fungal infections are well known. In this patient with severe immunologically compromised state (renal failure, diabetes, immunosuppressive therapy), the presence of epistaxis and periorbital oedema suggested a possibility of mucormycosis which was proved at autopsy.
The first case of mucormycosis was described by Paltauf in 1895 (as quoted by Gunson et al[5]). Since then many cases of rhinocerebral and systemic mucormycosis have been described. In majority of the patients, the diagnosis was made at autopsy[1] though many classical diagnostic signs have been stressed.[1] These include epistaxis, partial or total opthalmoplegia, chemosis and periorbital oedema, ptosis, exophthalmos etc. Other signs include greyish black discolouration of the nasal turbinates,[1] palatal ulcers[8] and frontal lobe signs.[8] Because of the haemorrhagic infarction of cerebral hemispheres with associated subarachnoid haemorrhage, features of cerebral oedema are also commonly seen.[8]
Various disease states have been reported to predispose to mucormycosis,[8] the commonest of these being diabetes, debilitating diseases (like leukemia, Kwashiorkar, marasmus), systemic malignancies,[1] prolonged use of antibiotics and immunologically suppressed states, including steroid administration. There are some reports of mucormycosis associated with renal failure.[1], [3], [7], [9] Of the three clinical varieties of mucormycosis viz. gastro-intestinal, respiratory, and rhinocerebral, the last one is seen most frequently. The route of entry of the fungus is through the nasolaryngeal and orbital passages into the intracranial cavity. There have been cases of mucormycosis associated with chronic renal failure,[3] acute tubular necrosis,[5] hepatorenal syndrome,[5] and various other diseases like glomerulonephritis, pyelonephritis and malignancy of the kidneys. The exact mechanism as to why these patients are susceptible to mucormycosis is not known. It is proposed that metabolic acidosis[3] and leukopenia in uraemia rather than the uraemic state are responsible. However, in some cases of mucormycosis with uraemia, metabolic acidosis was not evident. In most of the other diseases, the suppressed immunological state leads to invasion by mucormycosis.
However, the association of mucormycosis in stab wound cases,[5] coronary atherosclerosis, acute alcoholism and in many cases without any obvious disease remains to be explained.
The most striking mycopathological feature of mucormycosis is the vascular invasion by the fungi.[3] Vascular invasion is accompanied by thrombosis of the large and small arteries [Fig. 4] The veins are less frequently involved. As a result of extensive vascular thrombosis, cerebral haemorrhagic infarction is a constant finding in cerebral mucormycosis, as was evident in this case.
It is mentioned that "Amphotericin B" is the drug of choice.[4] However, this drug is excreted by the kidneys and is nephrotoxic. Hence its use in cases of renal failure is not without risk and makes the therapy more difficult.
The purpose of the present communication is to stress the association of mucormycosis with uraemia. Because an altered neurological state may result from variety of causes in a uraemic patient especially following hemodialysis, due importance must be given to the physical signs like epistaxis, periorbital odema, chemosis and opthalmoplegia so that a possibility of mucormycosis must b° suspected in such cases.
| 1. | Berk, M., Fink, G. I. and Uyeda, C. T.: Rhino-mucormycosis; report of a case diagnosed by clinical signs. J. Amer. Med. Assoc., 177: 511-513,1961.  |
| 2. | Cameron, J. S. and Ogg, C. S.: Rapidly progressive glomerulonephritis with extensive crescents. In, "Glomerulonephritis; Morphology, Natural History and Treatment-Part II." In, " Proceedings of the International Symposium" held at The Royal Melbourne Hospital, Australia, in Feb. 1972. Ed.-Kincaid-Smith, P., Mathew, T. H. and Lovell-Becker, E., John Wileys Sons, Melbourne, Australia, 1972, pp. 735-738. |
| 3. | Deshpande D. H. and Desai, A. P.: Cerebral mucormycosis in cases of renal failure. Neurology, India. 24: 20-23, 1976. |
| 4. | Goodman, L. S. and Gilman, A.: "The Pharmacological Basis of Therapeutics." 5th Edition, MacMillan Publishing Company, Inc., New York, Collier MacMillan Canada Ltd., Toronto and Bailliere Tindall, London, 1975. |
| 5. | Gunson, H. H. and Bowden, D. H.: Cerebral mucormycosis. Arch. Path., 60: 440443, 1955. |
| 6. | Hutter, R. V. P.: Phycomycetous mucormycosis in cancer patient-a complication of therapy. Cancer, 12: 330-350, 1959. |
| 7. | Kurrein, F.: Cerebral mucormycosis. J. Clin. Path., 7: 141-144, 1954. |
| 8. | LaTouche, C. J., Sutherland, T. W. and Telling, M.: Rhinocerebral mucormycosis. Lancet, 2: 811-813, 1963. |
| 9. | Neame, P. and Rayner, D.: Mucormycosis -A report on 22 cases. Arch. Path., 70: 261-268. 1960. |
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