World Journal of Pharmaceutical Research

Panneerselvam et al. World Journal of Pharmaceutical

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Volume 7, Issue 08, 977-982. Case Report ISSN 2277–7105

“NEONATE WITH DIGOXIN TOXICITY”

1
*Suganya Panneerselvam, 2Dr. Phalguni Padhi and 3Sharanabassappa Dambal

1
Msc (Psychiatric Nursing), Nursing Officer, All India Institute of Medical Sciences, Raipur,
Chhattisgarh.
2
MBBS, MD, DNB (Neonatology), Assistant Professor (Neonatology), All India Institute of
Medical Sciences, Raipur, Chhattisgarh.
3
Msc (Pediatric Nursing), Nursing Officer, All India Institute of Medical Sciences, Raipur,
Chhattisgarh.

Article Received on ABSTRACT

21 Feb. 2018, Digoxin is mostly used in the management of cardiovascular disorders.
Revised on 14 March 2018,
Accepted on 03 April 2018 It has narrow therapeutic index means that small variations in blood
DOI: 10.20959/wjpr20188-11871 concentration may easily result in toxic or subtherapeutic
concentrations. Prescribing digoxin and selecting a specific dose needs
*Corresponding Author to be done carefully. Here we present a case of a neonate who came to
Suganya Panneerselvam our hospital with a history of congestive cardiac defects and developed
Msc (Psychiatric Nursing),
digoxin toxicity. The serum digoxin levels were 4.5 ng/ml (normal
Nursing Officer, All India
range (0.8-2.0ng/ml) and it can be managed conservatively with close
Institute of Medical
Sciences, Raipur, monitoring.
Chhattisgarh.
KEYWORDS: Congenital heart disease, Digoxin Toxicity,
conservative management.

BACKGROUND
Congenital heart defects (CHDs) affect most of the neonates and it accounts for a high
proportion of infant mortality worldwide. There are regional differences in the prevalence
and distribution pattern of CHDs.[1] In India, the burden of congenital heart disease is
enormous, due to a very high birth rate.[2] The two defects in the heart, ventricular septal
defect (VSD) and atrial septal defect (ASD), account for about 30% of congenital heart
disease, among that VSD is the most common CHDs in infants and children which account
for 20% and ASD for 10%. These defects may occur as isolated lesions or as a component of
complex defects.[3] Ventricular septal defects occur in 0.1 to 0.4 percent of all live births.[4]

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Panneerselvam et al. World Journal of Pharmaceutical Research

The incidence of congenital heart diseases is reported in 7-9/1000 live birth with 1/6th to 1/4th
of these cases having critical congenital heart diseases. Therefore it is most important to
recognize this cause early and take initiative for proper treatments as it needs a specific and
urgent management. The late diagnosis can lead to significant respiratory compromises or
circulatory failure in up to 30% of non-syndromic children born with congenital heart
diseases.[5] Digoxin is mostly used in the management of cardiovascular disorders. Due to its
narrow therapeutic index, there is a high probability of accidental overdose leading to
toxicity. Serum digoxin levels below 0.8 ng/ml are considered subtherapeutic whereas, levels
more than 2.0 ng/ml may be toxic.[6]

CASE PRESENTATION
A full-term small for gestational age (SGA) male baby born by emergency Lower segment
Cesarian section (LSCS) due to oligohydramnios and meconium-stained amniotic fluid
(MSAF). The baby had delayed cry since birth, and he needed resuscitation with bag-mask
ventilation for 1 minute. The baby developed respiratory distress for which he was admitted
to neonatal intensive care unit in Industrial Hospital nearby. Initially treated for Meconium
aspiration syndrome. Respiratory distress kept on increasing and Chest X-ray revealed the
baby having cardiomegaly and the clinical findings were suggestive of congestive heart
failure. Due to unaffordability of the medical treatment by the parents, the baby was brought
to our super-specialty Government Hospital after 14 days of birth for further treatment.

On admission, vitals: temperature 36.5°C, pulse 176/min, respiratory rate 68 breaths/min,

capillary refilling time <3sec. Cardiovascular exam: S1, S2 sounds heard, Gallop rhythm,
pansystolic murmur. Respiratory exam: bilateral equal air entry and tachypnea. The baby also
had hepatomegaly, normal external genitalia, and no obvious congenital anomaly. The Chest
X-ray shows haziness with cardiomegaly, the echocardiogram shows large VSD and ASD, so
respiratory support given as continuous positive airway pressure (CPAP) for 72 hours after
that oxygen support given for 7 days. The baby also needed inotropic support and diuretic
therapy for CHDs with restricted fluid therapy. Sepsis screen came positive and blood culture
was sterile so the intravenous injections meropenem and vancomycin were given for 10 days.
The cerebrospinal fluid (CSF) was sterile. The lab investigations show the baby had low
platelet count 11,000/µL it reveals severe thrombocytopenia, so 30ml of platelet was
transfused immediately.

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The lab investigations after 10 days of admission shows Haemoglobin (Hb) 10.4g/dL, total
lymphocyte count (TLC) 8,500/µL, Platelets 2,88,000/µL, C-reactive protein 3.7mg/L,
Sodium 131.5mmol/l, Potassium 4.05mmol/l, Chloride 102mmol/l, thyroid stimulating
hormone (TSH) 3.20 µIU/ml. Cranial Ultrasound was done through the anterior fontanelle
window bilateral lateral ventricles and 3rd ventricles appear prominent with V/H ratio=0.39,
4th ventricle appears normal, Imaged part of the frontal, parietal and other parts of the brain
show normal echogenicity, no frank sonological evidence of the intraventricular/intra-
parenchymal bleed.

On the 10th day of admission, the respiratory rate becomes normal so, the oxygen (O2) was
tapered off. The sepsis screen result came negative. Bilateral hearing screening and the
neurological examination were normal. The baby was active, stable and accepted feeding was
required. So the baby was discharged after 15th day of admission with medications of
furosemide drops (10mg/ml) 0.3ml, Digoxin drops (50 mcg/ml) 0.2 ml, 5mcg on the1st day,
Enalapril tablets 0.1mg/kg, Phenobarbitone syrup (25mg/5ml) 2.5ml, Osteocalcium syrup
(82mg/5ml) 2ml, Tonoferon drops (25mg/ml) 5drops. The parents are instructed and
demonstrated regarding the digoxin toxicity and advised to bring baby after 15 days for
follow up.

DIGOXIN TOXICITY
The baby was brought again to hospital after 20 days of starting digoxin drops with a
complaint of bilious vomiting, abdominal distention, respiratory distress and lethargy in the
morning on the same day after administration of digoxin drop a few hours earlier. On
admission, the Vitals were: temperature 35.5°C, pulse 108/min, respiratory rate 50
breaths/min, capillary refilling time <3sec, blood pressure 52/30 (41) mmHg. Cardiovascular
exam shows pan-systolic murmur, S1&S2 sounds heard. The respiratory exam shows
bilateral equal air entry, liver 1cm palpable, normal external genitalia, and no obvious
congenital anomaly. Neurological examination shows poor rooting and sucking reflexes. His
abdomen was soft, bowel sounds were normal. The initial differential diagnosis was an
intestinal obstruction, septic ileus, dyselectrolytemia, and digoxin toxicity.

The lab investigations on readmission time shows Hb 9.1 g/dL, TLC 13,800 /µL, Platelets
2,24,000 /µL, C-reactive protein 9.8 mg/L, urea 175.5 mg/dl, creatinine 1.13 mg/dl, Sodium
141.3 mmol/l, Potassium 4.43 mmol/l, Chloride 109 mmol/l, blood culture shows methicillin
resistant coagulase negative staphylococcus antibiotic susceptibility.

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Serum digoxin level was 4.5ng/ml (normal range (0.8-2.0ng/ml). Once the toxicity confirmed,
digoxin drop was stopped immediately. The oral feed also stopped due to the danger of
aspiration, intravenous (IV) fluid ISO-P started, piptaz injection 250mg+10ml normal saline
IV over 1 hour started, furoped (10mg/ml) 5 drops BD. Oxygen (O2) was started by nasal
prongs to control respiratory distress. The parents of the baby couldn’t arrange digoxin
antibody due to financial problem. After 72 hours of admission, tachypnea was settled O2
was tapper off and full feed started through an oral-gastric tube, IV fluid stopped, gradually
the feed started through oral. The baby was started to settle down. At the 6th day of
readmission, the serum digoxin level was 0.5ng/dl. The baby has been discharged after 16
days from readmission with an advice to parents to continue oral feed, furoped drop
(10mg/ml) 5 drops, Calcimax 5 ml, HMI sachet (1gm)1/2 sachet in each 2 hourly feed, MCT
oil 3 drops in each feed, Syrup A-Z 1 ml, Syrup vitamin D3 5 ml, iron drop 5ml (10mg/ml)
and asked them to follow up after 1 week.

DISCUSSION
Digoxin has a narrow therapeutic index so if there is any small variations in blood
concentration it may easily result in toxic or subtherapeutic concentrations. So the blood
concentration is need to maintain within the therapeutic range it requires consistent
bioavailability and careful management of factors that may influence bioavailability.[7]

In neonate and young children it is difficult to identify the toxicity because they cannot
communicate their symptoms, so the specific symptoms may be missed out sometimes and it
lead to delay in diagnosis and make situation critical.[8] So, the prescribing and selecting a
specific dose needs to be done carefully. The parents and caregivers should be instructed and
demonstrated regarding the specific important guidelines for administration of the correct
dosing before discharge.[9] Giving drug holiday by not using digoxin on Saturday/Sunday
(popularly known as “5/7 therapy”) is another way to prevent digoxin toxicity without any
significant difference in its therapeutic effect.[10]

Digoxin toxicity includes cardiac and non-cardiac manifestations. The patient may either
develop brady or tachy-arrythmias. Electrocardiographic changes may include premature
ventricular contractions, atrial fibrillation or flutter, nonparoxysmal atrioventricular
junctional tachycardia or atrioventricular blocks.[6] Non-cardiac symptoms include anorexia,
nausea, vomiting and neurological symptoms. It can also trigger fatal arrhythmias.[11]

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One case here we have demonstrated that with provided that we can monitor vitals, have
electrocardiography facility and send digoxin level, it can be managed conservatively with
close monitoring. Although digoxin-specific antibody (Fab) is considered as the first-line
therapy and have been shown effective in safely and quickly eliminating digoxin from blood
and reduce mortality, it is not widely available in India and lot of patients cannot afford it. [12-
14]
Also the criteria for using digoxin-specific antibody fragments are unclear and serum
digoxin level alone may not be a good indicator.[15] There is no proper evidence-based
guidelines for the treatment of mild to moderate toxicity, so there is wide variation in the
management of digoxin toxicity.[16]

CONCLUSION
The management and monitoring the digoxin toxicity is still a challenging in some places due
to lack of proper evidence-based guidelines. It is needed to teach the parents, caregivers and
the medical staffs about digoxin toxicity.

AUTHOR’S CONTRIBUTION
Mrs. Suganya Panneerselvam: Involved in Nursing care, collection of data and drafting the
manuscript.

Dr. Phalguni Padhi: Physician treats the patient, provided critical revision and final approval
on the manuscript to publish.

Mr. Sharanabassappa Dambal: Involved in Nursing care and provided critical revision on the
manuscript.

ACKNOWLEDGEMENT
The authors express sincere thanks to the staffs of Neonatology department, All India
Institute of Medical Sciences, Raipur, Chhattisgarh for their support and guidance’s.

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