International Journal of Health Sciences and Research www.ijhsr.org ISSN: 2249-9571

Case Report

Recurrent in Pregnancy: Sweet Success

Bandar Naim Alamri1, Ali A A Y Mahmoud2, Shipra Kunwar3, Tamkin Khan4

1Intern, College of Medicine King Khalid University, KSA. 2Consultant, Abha Maternity and Children’s Hospital, MOH, Abha, KSA 3Associate Professor, Dept. of Obstetrics and Gynaecology, Era’s Lucknow Medical College, Lucknow, India. 4Associate Professor, Department of OBG, College of Medicine, King Khalid University, KSA.

Corresponding Author: Shipra Kunwar

Received: 19/01/2015 Revised: 14/02/2015 Accepted: 26/02/2015

ABSTRACT

Diabetic pregnancy is a high risk pregnancy associated with poor feto-maternal outcome. When poorly controlled it leads to Diabetic Ketoacidosis (DKA). A pregnant woman is more prone to develop DKA even at lower glucose levels. DKA increases the maternal and fetal morbidity and mortality by manifolds. Immediate recognition and aggressive management are essential to improve the feto-maternal outcome. Treating the underlying cause is important to prevent recurrence. Here we present a case of recurrent DKA [9 episodes] in pregnancy fortunately with a good outcome.

Key words: in pregnancy, diabetic ketoacidosis, lipohypertrophy.

INTRODUCTION CASE REPORT Diabetic pregnancy is a high risk A 22 year old Saudi female, G4P2+1, pregnancy associated with poor feto- live one and previous one IUFD , admitted maternal outcome. When poorly controlled, through ER with 29 weeks pregnancy with it leads to Diabetic Ketoacidosis (DKA) which the complaint of 5-6 episodes per increases feto-maternal morbidity and day for 2 days. Patient was a known case of mortality. DKA episodes in pregnancy may type 1 DM for past 12years, on insulin and be caused by hyperemesis, infections, non- had been admitted 9 times for DKA in the compliance, drugs etc. Here we report a case present pregnancy. The present pregnancy of recurrent DKA secondary to improper was a planned pregnancy. All admissions in administration of insulin. The case is this pregnancy were due to vomiting and reported for its rarity [9 episodes of DKA in pain abdomen under different consultants. same pregnancy], good feto-maternal The first admission was for hyperemesis and outcome by proper and aggressive DKA at 7 weeks gestation and subsequently management and for reiterating the there were 7 more admissions at 2-3 weekly importance of clinical examination in all intervals. She was noncompliant, always patients. presented to the ER, attended the endocrine clinic infrequently and was presumed to be

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negligent regarding her diabetes control and the cause of repeated episodes of antenatal care. However, on history she hyperemesis and DKA. denied missing any of her insulin doses or As she presented with vomiting we any dietary indiscretion. The husband were looking for a cause of hyperemesis and appeared to be supportive and both were recurrent DKA but could not get any extremely anxious for fetal wellbeing. There satisfactory explanation. Meanwhile, we was no history suggestive of any infective were joined by a new team member- an focus in the body or fever. intern who was asked to work up the case. Obstetric history: Her first pregnancy During examination of upper limbs he was a spontaneous abortion at 4 weeks. discovered bilateral lumps measuring 5×4 Second pregnancy was terminated by centimeters, firm, non tender in the deltoid caesarean section at 36 weeks for fetal muscles at site of insulin injections in both bradycardia, when a live girl, 2.5 kg was the arms. The patient had been self- delivered. Third pregnancy was IUFD at 36 administering insulin at the same site week due to DKA, delivered vaginally. continuously since her diagnosis of DM 12 On admission her examination years ago. Subsequently, the injection site revealed that patient was dehydrated, had was changed to abdomen and she was kept tachypnea 20/min, tachycardia 143 bpm and hospitalized for close feto-maternal hypotension 90/61 mmHg. The systemic monitoring. She received a course of examination was normal and obstetric steroids for fetal lung maturity. At 33 weeks examination revealed a 28 weeks sized she developed mild hypertension with uterus, relaxed, FHS normal. increasing albuminuria but did not have any Hb-11gm%, TLC-8200/cumm, DLC- new episode of DKA. Neutrophils-76%, lymphocytes-20%, Elective caesarean was done at 34 monocytes -04%, LFT –Normal, RFT- weeks and a live male baby was delivered. normal, blood glucose was 253 mg/dl , urine The baby weight was 1.9kg, placenta for 3+, urine for ketones-3+. Urine for weighed 300 grams and no congenital albumin was1+, Blood urea 19 mg/ dl, anomaly was present. Baby had an episode serum creatinine 0.9 mg\dl, sodium of mild respiratory distress and was admitted 132.3mmol/l, potassium 4.6 mmol/l, in NICU for two days. Mother and baby bicarbonate18.3mmol/l,O2 saturation was were doing well and discharged on request 94%, ABG revealed pH 7.3, PCO219mmHg, on 4th post-operative day. PO2 93.3 mmHg. HbA1C was 9.The fundus examination, chest radiograph and ECG DISCUSSION were normal, urine and blood cultures were The incidence of DKA has been negative. Cardiotocography was normal. reported as 1% to 10% from different Ultrasound revealed a live fetus, adequate studies. [ 1] While Cousins [ 2] reported an liquor and gestation age corresponding to incidence of 9.3% during 1965-85, recent her LMP. There was no fetal anomaly. and larger case series [ 3] reported it to be Thyroid function tests normal 1.2%.A pregnant diabetic is more prone to She was hospitalized in the high develop DKA as compared to a non- dependency unit and resuscitation started pregnant diabetic as normal metabolic with oxygen, aggressive intravenous fluids changes during pregnancy predispose to and insulin infusion. After maternal DKA. Majority of cases in pregnancy occur stabilisation and reversal of acidosis, patient in 2nd or 3rdtrimester, develop rapidly, at a was subjected to proper work up to explore lower blood glucose level and may not International Journal of Health Sciences & Research (www.ijhsr.org) 415 Vol.5; Issue: 3; March 2015

always manifest with the classic symptoms Correct injection technique is or laboratory findings. Maternal mortality important for insulin to be effective in from DKA has been reported between 4%– achieving glycemic control. Non-rotation of 15% from different studies. [ 4- 6] injection sites may result in localized Fetal loss rates may be as high as lipohypertrophy, degeneration or atrophy 10–25% for a single episode of DKA despite causing unpredictable and delayed substantial improvements in perinatal and absorption. Patient counseling regarding neonatal care. [ 7] injection technique at first visit and audit at Hyperemesis, infection, non- each subsequent visit is essential. [ 12, 13] compliance, insulin pump failure, β- Insulin injection site amyloidosis and zinc sympatheto-mimetic and corticosteroids for granulomas have also been reported preterm labor alongwith poor management affecting absorption kinetics. [ 14- 16] may be the precipitating factors. [ 8] Making a diagnosis is a step wise Symptoms of DKA are polyuria, process involving information gathering and polydipsia, nausea, vomiting, abdominal generating a hypothesis. Data acquisition pain, weakness, weight loss. Signs include begins with history, clinical examination and hyperventilation, ketotic breath, tachycardia, investigations. [ 16] hypotension, disorientation or coma. [ 7- 9] However in recent times we have Prompt recognition and management forgotten this stepwise approach –the of this medical emergency is essential in investigations are ordered without order to optimize feto-maternal outcome. examination and many a times the diagnosis Finding the underlying cause is important. A is missed or delayed because of this. careful history and physical examination We were able to find the underlying may elicit the precipitating cause or may cause of recurrent DKA as lipohypertrophy identify non-compliance with medical on examination. This reiterates the therapy. [ 9] importance of physical examination in Our case of DKA presented as making a diagnosis. nausea and vomiting as early as 7 weeks and Importance of physical diagnosis has been was labelled as hyperemesis gravidarum emphasized right from the time of [HG]. Each time she was admitted we were Hippocrates [460-370 B.C] to Laennec looking for a cause of HG investigating her [1816] to Osler. [ 17] for the same even in later pregnancy though A study found that 90% of HG rarely persists beyond 20 weeks. [ 10] physicians believed that physical The differential diagnosis of examination is important in patients of hyperemesis gravidarum includes urinary hypertension and rheumatology but only tract infection, uremia, thyrotoxicosis, laboratory tests were enough for diagnosis diabetic ketoacidosis, Addison disease, and management of diabetes mellitus and hypercalcemia, gastritis, peptic ulcer hyper-cholesterolemia. [ 18] However cases disease, , bowel obstruction, like ours prove that physical exam is and hepatitis drug-induced vomiting, central will remain important for diagnosing disease nervous system (CNS) disease, and and developing the patient-doctor vestibular disease. [ 11] relationship. [ 19] Inspite of all investigations and USG In Osler's words “Learn to see, learn we could not find a cause which was later to hear, learn to feel, learn to smell and elicited by history and examination. know that by practice alone can you become experts”. [ 20] The combination of a good International Journal of Health Sciences & Research (www.ijhsr.org) 416 Vol.5; Issue: 3; March 2015

history, thorough physical examination Gravidarum, Rev Obstet Gynecol. along with the correct use of investigations 2012;5(2):78-84. can help us become better diagnosticians to 11. Kalra S, Balhara YP, Baruah MP. provide the best care to our patients. Forum for Injection Techniques, India: The First Indian REFERENCES Recommendations for Best Practice 1. Parker J A, Conway D L. Diabetes in Insulin Injection Technique Indian ketoacidosis in pregnancy: Obstet J EndocrinolMetab. 2012 Nov-Dec; Gynecol Clin North Am. 2007;34: 16(6): 876–85. 533–43. 12. Frid A, Hirsch L, Gaspar R et al; 2. Cousins L. Pregnancy complications New injection recommendations for among diabetic women: review, patients with diabetes. Scientific 1965-1985. Obstet Gynecol Surv Advisory Board for the Third 1987;42:140–9. Injection Technique Workshop. 3. Schneider MB, Umpierrez GE, Diabetes Metab. 2010 Sep;36Suppl Ramsey RD, et al. Pregnancy 2:S3-18. complicated by diabetic 13. Kudo-Watanuki S, Kurihara E, ketoacidosis: maternal and fetal Yamamoto K et al. Coexistence of outcomes. Diabetes Care 2003;26: insulin-derived amyloidosis and an 958–9. overlying acanthosisnigricans-like 4. Confidential enquiries into maternal lesion at the site of insulin injection. deaths:1979–1981, 1982–1984, Clin Exp Dermatol. 2013 Jan;38 1985–1987, and 1988–1990. (1):25-9. London: Department of Health, UK. 14. Jordaan HF, Sandler M. Zinc- 5. Gabbe SG, Mestman JH, Hibbard induced granuloma--a unique LT. Maternal mortality in diabetes complication of insulin therapy. Clin mellitus: an 18-year survey. Obstet Exp Dermatol. 1989;14(3):227-9. Gynecol 1976;48:549–51. 15. Albert SG, Obadiah J, Parseghian 6. Goto Y, Sato SI, Masuda M. Causes SA et al. Severe insulin resistance of death in 3151 diabetic autopsy associated with subcutaneous cases. Tohoku J Exp Med. 1974; amyloid deposition. Diabetes Res 112:339–53. ClinPract. 2007 Mar;75(3):374-6. 7. DeVeciana M, Diabetes ketoacidosis 16. Hatala R, Smieja M, Kane SL, Cook in pregnancy. Semin Perinatology DJ, Meade MO Nishi Kawa J. An 2013 37(4):267 –73. evidence based approach to the 8. Kamalakannan D, Baskar V, Barton clinical examination, J Gen Intern DM, et al. Diabetic ketoacidosis in Med, vol 1 march 1997;12(3)182-87. pregnancy. Postgrad Med J. 2003;79: 17. Walker HK. The Origins of the 454-57 . History and Physical Examination. 9. Jueckstock JK, Kaestner R, Mylonas In: Walker HK, Hall WD, Hurst JW, I. Managing hyperemesis editors. Clinical Methods: The gravidarum: a multimodal challenge History, Physical, and Laboratory BMC Medicine 2010; 8:46. Examinations. 3rd edition. Boston: 10. Wegrzyniak LJ, Repke JT, Ural SH. Butterworths; 1990. Chapter 1. Treatment of Hyperemesis Available from:

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How to cite this article: Alamri BN, Mahmoud Ali AAY, Kunwar S et. al. Recurrent diabetic ketoacidosis in pregnancy: sweet success. Int J Health Sci Res. 2015; 5(3):414-418.

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