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Obgyn #26

28-year-old woman comes to the clinic at 29 weeks gestation complaining of headaches and abdominal pain. She states that these symptoms began 5 days ago and have been worsening.  The patient's vitals are notable for a blood pressure of 175/95 mmHg.  On physical exam pain is elicited upon palpation of all 4 quadrants, in particular the right upper quadrant.  A urine dipstick demonstrates 3+ protein.  The patient is admitted to the hospital and started on IV magnesium sulphate and labetalol.  Five hours after this treatment has begun she has a seizure.
What is the next best line of mangement?

A.    Start IV lisinopril
B.    Observe expectantly and deliver only if the              patient shows signs of seizure
C.   Deliver promptly
D.   Start sumatriptan
E.   Start IV magnesium

Answers and Explanations
DISCUSSION: The patient is presenting with classic signs and symptoms of severe preeclampsia with end-organ damage, which requires immediate delivery as treatment.
Severe preeclampsia (BP > 160/110 and 3-4+ urine dipstick protein) with evidence of end-organ damage, including headache, epigastric pain, disseminated intravascular coagulation, oliguria, or pulmonary edema, is an obstetrical emergency that is managed by delivery regardless of gestation age. If no end-organ damage is present, it is possible to monitor the patient in an ICU setting until 32 weeks gestation, when delivery is indicated regardless of end-organ damage. IV magnesium sulfate may be given for seizure prophylaxis. The onset of preeclampsia occurs from 20 weeks gestation to 6 weeks postpartum. If symptoms occur before 20 weeks, consider a molar pregnancy as a cause of hypertension.
Key steps in the management of all types of hypertensive disorders of pregnancy. Risk factors include preexisting hypertension, nulliparity, maternal age of < 20 years or >35 years, diabetes, chronic renal disease, or autoimmune disorders.
Aloizos et al. discuss the management of pre-eclampsia. Delivery is the only definitive treatment for pre-eclampsia/HELLP syndrome. Delivery is indicated after 35 gestational weeks or the fetal and/or maternal conditions deteriorate. Furthermore, vaginal delivery is preferred.

Endo #121

A 22-year-old female was taken to the emergency room in coma. Her parents noticed that she had for the past 1 month polydipsia, polyuria, and rapid weight loss. These symptoms had worsened in the last week. She had not been taking any medications and the clinical history was otherwise unremarkable. On examination, breathing was deep and rapid (Kussmaul respiration), pulse rate was 104 beats per minute, and blood pressure 110/70 mmHg; she also revealed a mildly dehydrated patient. She was drowsy and confused. Rapid hematology and biochemical tests showed
Hematocrit 46%
Hemoglobin 13 g/dl (140 g/L)
White blood cell count 11,000/ μl
Glucose 520 mg/dl (28.9 mmol/L)
Urea 50 mg/dl (8.5 mmol/L)
Creatinine 0.8 mg/dl (70.7 μmol/L)
Na+ 148 mEq/L
K+ 4.6 mEq/L
PO4 3-2.0 mEq/L (0.64 mmol/L)
Cl− 112 mmol/L
Arterial pH was 7.0
PO 2 98 mmHg
PCO 2 25 mmHg
HCO 3−12 mEq/L
O 2 sat 98%.

What’s the diagnosis?
A.  Cerebral edema
B.  Rhabdomyolysis
C.  Acute pancreatitis
D.  Sepsis
E.  Acute abdomen
F.  Diabetic Ketoacidosis
G. Alcoholic ketoacidosis

Answers and Explanations   F
The patient has marked hyperglycemia and metabolic acidosis. The diagnosis of newly diagnosed type 1 diabetes presenting with DKA should be considered.

Diabetic ketoacidosis (DKA)
·        Cause: severe insulin deficiency. Cell begin to shift to lipolysis, which results in the creation of ketone bodies. This causes acidemia (Anion gap metabolic acidosis). Often precipitated by inflammatory process, medication non-compliance, illicit drug use.
   Sx: Polyuria, Polydipsia, N/V, malaise, fatigue, Tachypnea, Palpitations, Abdominal Pain, reduced appetite, LOC
       Px: Dry skin/MMs, reduced skin turgor, hypotensive, tachycardic, confused, ill-looking patient
       Dx: Clinical, most important labs are fingerstick glucose, UA+dipstick, CMP, CBC, ABGs, cultures, also should get an EKG, serum level of hydroxybutyrate.
 Glucose: Will always be>250mg/dL, often much higher
  CBC: WBC will be increased regarding of whether there is an underlying infection or not. A left shift suggests infection. Should culture blood
 UA: dipstick will be highly positive for glucose, ketones, UA will confirm this. *Urine culture should be performed.
CMP: Hyperkalemia, Hyponatremia, low bicarbonate, High anion gap suggesting the unfavorable anion gap metabolic acidosis.
   ABGs: Metabolic acidosis
  Hydroxybutyrate: High

DKA Management:
Goals in therapy are to replenish depleted fluid volume and to replace insulin,   keeping a keen eye on the serum electrolytes.
·         Correction of fluid loss with intravenous fluids.  IVF, in adults, rapid infusion of 1L of 0.9% NS (e.g. over 30 min), repeat bolus as necessary to prevent shock.
·         Correction of hyperglycemia with insulin In newly diagnosed patients with type 1 diabetes, a careful estimate of the long-acting insulin dose should be considered. Starting with smaller doses generally is recommended to avoid hypoglycemia. (SC long-acting insulin (eg, insulin glargine, Detemir) should be initiated at the dose that was used prior to the manifestation of DKA). Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL.
·         Correction of electrolyte disturbances, particularly potassium loss. Ensure potassium level of >3.3 mEq/L before initiation of insulin therapy (supplement potassium intravenously if needed). If initial K >6, then withhold replacement. If K< 4.5, then administer 10-20 meq/hr of K. If initial K < 3, then administer 40 meq/hr
·         Correction of acid-base balance. If pH < 7.1 and/or cardiac instability present, then give bicarb.
·         Treatment of concurrent infection, if present
·           If K > 6.0, administer no K
·           If K = 4.5 – 6, administer 10 mEq/L KCI
·           If K = 3- 4.5, administer   20 mEq/L KCI
·           If K < 3, stop insulin

 Treat underlying cause
 Bicarbonate is only given with severe academia (usually the wrong answer)
 After the emergent treatment, underlying cause should be found
      Pt should be admitted, put on a sliding scale (while underlying cause is searched for/treated)
     May discharge when pt. can take daily insulin regimen and the underlying cause is resolved.
     Must emphasize the importance of adhering to a strict insulin regimen.
*Treatment of DKA includes: (Normal saline, Potassium, Insulin and Glucose, Treatment of the precipitating event as appropriate)


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