A 25 year old primigravida presented to the gastroenterologist at 26 weeks' gestation with complaints of 10-12 episodes of diarrhea and increased thirst for a duration of 2 months. No history of fever. She was apparently drinking about 8-10 L of water everyday and was still complaining of dryness of mouth and thirst and weakness. She was from a rural area with limited access to medical aid.
Day 1: She was referred to me to check on fetal status. Fetus was normal size and heart beat was around 150bpm. A renal profile and complete blood count was requested. She was treated for gastroenteritis and blood sugar was 132mg/dl. Blood pressure was normal at 110/80mmHg. Amylase 62U/L(0-80), Urea 15mg/dl(15-40), Creatinine 0.5mg/dl(0.6-1.6), Hb 10.4g%(11-16.5), WCC 8,800/cumm(4000-11000). Na147mEq/L(135-146) and K 2.9mEq/L(3.5-5.5) and chloride 113mEq/L(95-105). By the end of first day of admission, she had one episode of diarrhea. Strict input/output chart was being maintained. Ultrasound scan showed a live intrauterine singleton pregnancy of 31 weeks' gestation, liver, GB, pancreas, kidneys were normal looking. Urine for ketone bodies was negative.In a 17hour period, she had passed, 3.5L of urine and intake was 5.8L.
Day 2: Electrolytes were repeated and by next morning she had 8 episodes of diarrhea, no vomitings and intake of fluids at 4litres in 9 hours. Stool and urine were sent for culture and sensitivity. Iron, calcium and antacids were stopped. Fluids were restricted to 2L per day on day2 as it has been observed that excess fluid intake can be a cause of diarrhea. Diarrhea continued, sodium was now raised at 154mEq/L and potassium at 3.3mEq/L, Chloride 123mEq/L. Urine and serum osmolality was requested. Urine osmolality was 77.6mosm/kg(300-850 mosm/kg). Serum osmolality was 396.2mosm/kg(280-295) Thyroid function tests were normal. She passed stools about 20times that day. Her urine was very clear on inspection. She was asked to restrict her fluid intake and staff were asked to give her a bedpan to pass stools to notice any abnormality. She was very desperate for water in the night to the point of being abusive to the hospital staff and her urine remained very dilute. Input 3.8L and output 2.9L.
Day 5: DDAVP was continued. Electrolytes Na 142, K 3.1,Urine output 70-150ml/hr.Input 1.25L, Output 1.1L. A diagnosis of Diabetes insipidus in pregnancy was made. Her diarrhea was due to excess water intake.
She was discharged on the sixth day after admission. She was warned of recurrence in next pregnancy and to seek early medical attention.
Diabetes insipidus is a very rare condition and even rarer in pregnancy with an approximate incidence of 1 in 30,000 pregnancies. These women have either decreased central secretory reserve or impaired renal responsiveness to vasopressin. In addition, women can experience diabetes insipidus de novo in pregnancy through the actions of placental vasopressinase, which causes accelerated degradation of vasopressin. This form of diabetes insipidus may be associated with increased complications of pregnancy, including preeclampsia. DDAVP cannot be degraded by placental vasopressinase and is the treatment of choice.
Day 1: She was referred to me to check on fetal status. Fetus was normal size and heart beat was around 150bpm. A renal profile and complete blood count was requested. She was treated for gastroenteritis and blood sugar was 132mg/dl. Blood pressure was normal at 110/80mmHg. Amylase 62U/L(0-80), Urea 15mg/dl(15-40), Creatinine 0.5mg/dl(0.6-1.6), Hb 10.4g%(11-16.5), WCC 8,800/cumm(4000-11000). Na147mEq/L(135-146) and K 2.9mEq/L(3.5-5.5) and chloride 113mEq/L(95-105). By the end of first day of admission, she had one episode of diarrhea. Strict input/output chart was being maintained. Ultrasound scan showed a live intrauterine singleton pregnancy of 31 weeks' gestation, liver, GB, pancreas, kidneys were normal looking. Urine for ketone bodies was negative.In a 17hour period, she had passed, 3.5L of urine and intake was 5.8L.
Day 2: Electrolytes were repeated and by next morning she had 8 episodes of diarrhea, no vomitings and intake of fluids at 4litres in 9 hours. Stool and urine were sent for culture and sensitivity. Iron, calcium and antacids were stopped. Fluids were restricted to 2L per day on day2 as it has been observed that excess fluid intake can be a cause of diarrhea. Diarrhea continued, sodium was now raised at 154mEq/L and potassium at 3.3mEq/L, Chloride 123mEq/L. Urine and serum osmolality was requested. Urine osmolality was 77.6mosm/kg(300-850 mosm/kg). Serum osmolality was 396.2mosm/kg(280-295) Thyroid function tests were normal. She passed stools about 20times that day. Her urine was very clear on inspection. She was asked to restrict her fluid intake and staff were asked to give her a bedpan to pass stools to notice any abnormality. She was very desperate for water in the night to the point of being abusive to the hospital staff and her urine remained very dilute. Input 3.8L and output 2.9L.
Day 3: By morning, she started to get drowsy. Pt appeared very dehydrated. One episode of diarrhea at night. Passed urine 3 times. Electrolytes were repeated urgently and sodium was 190mEq/L, potassium 3.2mEq/L. She was developing cerebral edema due to electrolyte imbalance. She was given 1/2 NS, Frusemide 40mg iv. Urine output was 1.8L, very dilute.Rapid infusion of fluids in Intensive care was started. 2.5L of half normal saline with a potassium sparing diuretic, Spironolactone was given and Desmopressin (DDAVP) nasal spray was started. Blood gases were done at 8am: pH:7.3, pCO2 17mmHg, pO2 107mmHg, Na 180 mEq/L, K 3.7mEq/L. Ultrasound scan repeated showed intrauterine fetal death. Repeat electrolytes showed Na 163, K 4.2, Cl 134. Input 7.6L, Urine output 3.8L. She continued to have polydipsia despite oral fluid intake of 0.9L and IV fluids of 4L. Lungs were clear. DDAVP was given as 20µg each nostril. By 8pm she was stable and was having tightenings of the uterus. At midnight,Electrolytes Na 143, K 3.4, Cl 113
Day 4: At 6 am, Electrolytes Na 143, K 3.8, Cl 114 Misoprostol induction of labour was started at 9am and she went on to deliver a stillborn female baby at 5pm. Thirst was reduced. Input: 5.3L, Output:L 3.7L.
She was discharged on the sixth day after admission. She was warned of recurrence in next pregnancy and to seek early medical attention.
Diabetes insipidus is a very rare condition and even rarer in pregnancy with an approximate incidence of 1 in 30,000 pregnancies. These women have either decreased central secretory reserve or impaired renal responsiveness to vasopressin. In addition, women can experience diabetes insipidus de novo in pregnancy through the actions of placental vasopressinase, which causes accelerated degradation of vasopressin. This form of diabetes insipidus may be associated with increased complications of pregnancy, including preeclampsia. DDAVP cannot be degraded by placental vasopressinase and is the treatment of choice.
You might want to add some research findings at the end of your case, when u find time to do so.
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