Summer complaints and homoeopathy management

Dr Aadil Chimthanawala

Time passes, summer comes and goes. But there are few moments that also teach us something, provided we are susceptible to learning. Such an educative experience happened with us in this summer of 2009. It was in the form of 2 neonates born on the same day and practically at the same time of different parentage who had battled for life just after birth.

One was victorious but the other sadly lost. In the process of management of these two cases, several lessons were learnt that would go a long way in deciding numerous aspects of homoeopathic management in new born children. It is these lessons that I wish to share with the homoeopathic fraternity.

Ravi – a 7 days old male child, was referred to us with complaints of –
1. Vomiting, recurrent abdominal colic and loose motions – since 4 days
2. Convulsion – 3 days ago.

Ravi is the first male child (after 2 female siblings) of a non-consanguinous marriage. He was delivered vaginally at a local village (Bhandara) nursing home at 39 weeks gestational age (22/4/09). At delivery, he had good APGAR score of 9 at 1 minute with a good cry. He was seen by a pediatrician and discharged the 2nd day. He was feeding well on breast milk since birth for 2 days when on every feed he started having non projectile vomiting of curdled milk, abdominal colic followed by loose motions that were sour, offensive frothy and with fatty masses. He was hospitalized and started on cow’s milk with parental fluids and an antibiotic. Serum Calcium / Glucose levels were within normal limits. 1 day after admission symptoms continued. In addition, he had a single generalized seizure with heavy breathing. Hence he was referred to a tertiary center at Nagpur.

On admission, he was afebrile with weight-2.86Kg, length-42cm & head circumference-31cm. He had spontaneous movements and a good sucking reflex. He had good eye opening but startled on slightest touch. There were no abnormalities noted in the head or neck and he had no respiratory distress. He had regular heart rhythm with dual heart sounds and no murmur. His pulses were easily palpable. He had no pallor, icterus or cyanosis. His abdomen was soft, non distended. Liver was enlarged 3.5 cm but non tender. No other organomegaly was present. On neurological examination there was good movement of all the limbs and sensory examination revealed him to withdraw the soles normally. He underwent a chest x-ray that was normal and an abdominal sonography that was essentially normal with mild hepatomegaly.

His blood counts, RBC indices, haemoglobin, stool & urine examination ruled out septicemia or enterocolitis. Blood gas pH was 7.33 and PCO2 of 41. All his serum electrolytes & creatinine were within normal limits. Blood urea was 9.8mg /dl, Serum Ammonia was 490mg/dl (Normal 50-150mg/dl) and Total Bilirubin was 4.2mg/dl.

F/H – Ravi has 3 maternal aunts. The male children of all the three died within 1-3 weeks of their respective births. Maternal grandmother died – Astrocytoma.
Following symptoms were considered
1. Vomiting, curdled milk,
2. Abdominal colic
3. Stools – loose, sour, offensive frothy, fatty masses with
4. Startled < slightest touch
5. Liver enlarged
On repertorisation the set of medicines that came out were – Arsenic alb, Mag carb, Verat alb, Aethusa
27/4/09 Blood sent for R/o Urea Cycle Enz NBM + Dextrose 5% @ 80mg/kg/d
deficiency or amino acid dysfunc Mag carb 30 3 hourly
28/4 Vitals stable. No Vomit /colic Mag carb 30 TDS
29/4 Started oral feed- glucose water Mag carb 30 BD. Omit IV Fluids
30/4 Started breast feed. No vomit/LM No IV Fluids
S.Ammonia 78 mg/dl
1/5 Patient >> No meds
2/5 S. Ammonia 61mg /dl
3/5 On discharge, Ravi was stable on room air throughout his stay. He had remained stable from a cardiovascular standpoint –never evidencing a murmur on exam. He has been breast feeding well every 3 hours with no emesis, loose motions or convulsion. He had no evidence of any infectious disease. His mother’s blood group is ORh+ and Ravi’s blood group is A+ and thus they are potential set for ABO incompatibility. Bilirubins were monitored for 1 week but they were within normal limits. Pink, active baby with weight 2.5 Kg, Temp 36.7, HR 144/min, RR 36/min, BP 78/41 mmHg.. Liver-palpable 2.4 cms. Neuro– alert, responsive and patellar reflex present bilaterally. The results of the work-up done to rule out enzyme deficiency were normal.
Final Diagnosis – Transient Hyper-ammonemia of Newborn.

I was called to visit 9 days old Saurabh at a Neonatal ICU of Nagpur. The baby was on Ventilator and was diagnosed as severe pulmonary hypertension. He was the 1st child of a non-consanguinous marriage and was delivered vaginally at 36 weeks gestational age (22/4/09). At delivery he cried immediately but aspirated the meconium. He went into severe apnea with bradycardia. He was resuscitated with Ambu bag. Although the respiration became spontaneous in 1 minute but the distress continued. He was put on ventilator with an FIO2 requirement of 60%, respiratory rate at 50/minute. X-Ray Chest showed bilateral generalized haziness. 2D ECHO- severe pulmonary hypertension (PASP =55mmHg) + Good Left ventricular Function (EF=60%) + small PDA with non restrictive bi-directional shunt. No Pulmonary Artery / Aortic stenosis or regurgitation. Right Atrium /Ventricle dilated. Inter-atrial septum had a patent foramen ovale with right to left shunt.

Serum Calcium/Glucose levels were normal. Blood gases–acidosis, Liver & kidney functions were within normal limits. USG abdomen was also normal. His blood counts, RBC indices, hemoglobin, stool & urine examination ruled out septicemia. He was on antibiotics, slidenafil citrate and parental feeds. 8 days after admission there was no relief except a little resolution of the pneumonia. Hence the pediatrician asked for homoeopathic help.

When I examined the baby, he was afebrile with a weight of 2.2 Kg, length of 40 cm and a head circumference of 29 cm. He was on ventilator, looked pale and there were no spontaneous movements. The skin was an-icteric and acyanotic. His abdomen was soft, non distended with no organomegaly. FIO2 was 100%, PCO2 55, respiratory rate was set on the ventilator to 72/min. In this artificial setting, following symptoms were considered

  • Asphyxia neonatorum
  • Breathing difficult, pulmonary edema in
  • Breathing difficult, heart problems with
  • Breathing difficult, lung cannot expand
  • Breathing difficult, mucus, in trachea (lungs) from
  • Rattling chest

Following medicines came out prominently – Antim tart, Carbo Veg, Laurocerasus, Aconite Ferox
1/5/09 Antim Tart 0/1 inhalation 1 hourly
11 am

1/5 9pm Vitals stable. FIO2 92%, R/R 60 Antim Tart 0/2 TDS inhalation
2/5 Vitals as above. X-chest – Haziness Antim T 0/2 BD. Omit Sildenafil
less. IVF contd.
3/5 Feeding via Nasogastric Tube+ Antim T 0/2 BD ct.
FIO2 80%, R/R 50/min
4/5 Pt. same. Vent parameters same Antim T 0/3 3h
5/5 No change in status. R/R 74/min Aconite F 0/1 x 1h inh
6/5 FIO2 46%, R/R 40/min Aconite F 0/2 x TDS
7/5 Pt. Set for weaning from Ventilator Aconite F 0/2 TDS
8/5 Spontaneous breathing achieved Aconite F 0/2 BD
Pt was weaned well.
9/5 Sudden cardio- respiratory arrest CPR given but failed.

Lessons learnt

1. As physicians our first duty is to save the life of the patient. As homoeopaths, we should dare to accept such challenges of tackling medical emergencies.

2. Hyperammonaemia is a metabolic disturbance characterised by an excess of ammonia in the blood. It may lead to encephalopathy and death. It may be primary or secondary. Ammonia is a substance that contains nitrogen. It is a product of protein catabolism. It is converted to the less toxic substance urea prior to excretion in urine by the kidneys. The metabolic pathways that synthesise urea are located first in the mitochondria and then into the cytosol. The process is known as the urea cycle, which comprises several enzymes acting in sequence. Primary hyperammonemia is caused by inborn errors of metabolism that are characterised by reduced activity of any of the enzymes in the urea cycle like ornithine transcarbamylase, glutamate dehydrogenase 1, ornithine translocase and N-acetylglutamate synthetase.

3. Secondary hyperammonemia is caused by inborn errors of intermediary metabolism characterised by reduced activity in enzymes that are not part of the urea cycle (e.g .Propionic acidemia, Methylmalonic acidemia) or dysfunction of cells that make major contributions to metabolism (eg hepatic failure).

4. Miasmatically, this transient but violent episode in Ravi, luckily was a psoric disorder hence responded well to a few doses of Mag carb only. The baby was able to feed on its mother’s milk hardly within a week. It has been found that single Enzyme deficiency states are sycotic and are incurable. The treatment centers on limiting intake of ammonia and increasing its excretion. Dietary protein (a source of ammonium) is restricted and caloric intake is provided by glucose and fat. The laboratory studies indicated in ruling out these sycotic states are – Plasma ammonia, Liver function test (S.transaminases, prothrombin time/activated partial thromboplastin time, alkaline phosphatase levels, S. bilirubin), Plasma amino acid level quantitation, Urinary organic acid profile, Urine amino acid levels, Blood lactate, Blood gas (alkalosis) and BUN. In our case, the cause for hyper ammonemia is unidentifiable.

5. In the second case, although Saurabh was weaned from the ventilator albeit for 32 hours yet the baby died due to cardio-respiratory arrest. Antim Tart was selected and it gave enterprising results for the 1st 4 days. Then the response stagnated even though the potency was increased, rather the respiratory rate and FIO2 increased. It was Aconite Ferox that gave us the chance for weaning the patient off the ventilator. The decision was clinical. Saurabh was a preterm baby with meconium aspiration and the prognosis was already explained to his relatives.

6. In our experience, when we compare Aconite Ferox versus Carbo veg & Laurocerasus, we have found that the indications for the 3 remedies are very similar except that Carbo Veg & Laurocerasus predominantly have cyanosis with respiratory paralysis where as it is absent in Aconite F. Hence it was chosen.

7. When homoeopaths have to work in such set-ups of modern medicine (ICCU / NICU), the drug selection becomes dicey since time is less, the settings are artificial, there are hardly any natural symptoms to prescribe upon, the patient is already on a good number of allopathic medications, the homoeopathic help is resorted at a stage when the pathology is far advanced and the allopathic medications have failed to act. But for saving the life of the patient, one needs to join hands. Even if the homoeopathic remedy selected is a partial or a pathological similimum (as in our case), the situation demands us of extending a helping hand. God knows! Miracles do happen.

Dr. Aadil Chimthanawala  MD (Hom), DNB (Med), MBBS, BHMS, FNAHI, PGNAHI
Secretary: National academy of homoeopathy, india, Homoeopathic Cardiologist

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