Black Water Fever.
NATIONAL JOURNAL OF HOMOEOPATHY 1994 Sep / Oct Vol III No 5.
Praveen Kumar.

This is otherwise known as malarial haemoglobinuria which is a new and dangerous complication of Plasmodium Falciparum malaria occurring in non-immune residents of malarious areas though its cause is obscure. The abused drug quinine may precipitate an attack. Primaquinine may also play a part in initiating the disorder in individuals with G6PD deficiency (Glucose 6 Phosphate dehydrogenase).

There will be a sudden, extensive intravascular haemolysis. This could be due to an immunity reaction where red cells of the patient produce a certain auto-antigen. This stimulates production of an anti-haemolysis which sets off the disaster.

Degenerative changes occur in the epithelium of the tubules of the kidneys. The dangerous complication of BWF could be due to renal failure, not due to blockage of the tubules by debris, but due to changes in intra-renal blood flow, cortical ischaemia and anoxia.

If a physician can make a correct diagnosis of the pre-black water fever state, it could pull the patient out of a catastrophe. In this case there will be a history of fever and conjunctiva appear icteric. The liver is enlarged and tender and the spleen is palpable. Blood examination reveals a few subtertian malarial rings. At this stage if proper treatment is given, BWF may not set in.

The onset of haemolysis is very sudden and abrupt. In one of the bouts of fever the patient suddenly feels severe pain in the loin and gets a constant urge to pass urine. He is shocked to find his urine almost black. This gives the disease its name. The urine may pass through several shades from near normal color to dark brown or cherry red or black. There may be bilious vomiting and intense epigastric pain the liver becomes very tender on palpation. Skin may appear pale and later take on a saffron tint. Hemorrhagic symptoms may appear if renal failure ensues; sudden syncope, coma or convulsion could occur.

Lab Findings:

1. Presence of Haemoglobin in plasma and urine
2. Methaemoglobin is also present in plasma.
3. Urine - contains much albumin and could become solid on boiling. On settling, the urine is seen to consist of two layers an upper layer and a lower brownish grey sediment containing tube casts and some erythrocytes.
4. CBP - sudden diminution in RBC count with normal RBC fragility. Presence of few ring forms in peripheral smear. In many patients parasitaemia is absent during haemolysis. Vanderbergh usually indirect positive.
5. Raised blood urea, spectroscopic examination reveals presence of oxyhaemoglobin.

Diagnosis:

1. History of fever and rigors, pain in the loin, passing blackish urine.
2. Onset of oliguria or anuria.
3. Lab reports of urine and blood as described above.

Complications:

1. Acute Renal Failure
2. Hyper-pyrexia with convulsions and coma
3. Cholelithiasis
4. Anaemia and debility.

Treatment:

As the prognosis is not good in severe cases which will have 50 percent mortality, early diagnosis and prompt treatment are key factors.

Complete bed-rest, fluid infusion and if necessary blood transfusion would go a long way in the management of the case.

Homoeopathic Drugs: Acid-nit, Carb-ac, Colo, Lach and Terebinth are the leading remedies apart from Ars, Nat-m, Canth and Phos.

The other important point to be always kept in mind is its recurrence and survivors may experience haemolytic episodes. Hence there should be a frequent check-up of the patients even after complete recovery.