Morbidity and Mortality

1. NeuroICU Nurse Practitioner Conference Morbidity and Mortality

2. Identifying Information • Mrs. D is a 30 year old woman with a 1-year history of worsening headaches and visual field defects. MRI showed large cystic lesion extending from suprasellar region to the ventricles, with rim enhancing multiloculated tumor in hypothalamus. Now DOS s/p resection. Uneventful surgical course except for bradycardia during traction on the carotid, and slow emergence necessitating narcan.

3. History PAST MEDICAL HISTORY PAST SURGICAL HISTORY C-Section 2003 Tubal ligation 2004 • Hypertension • Craniopharyngioma

4. Physical FindingsImmediately Post-Op • NEURO: Sleepy but arousable. AOx3. f/cx4 with 5/5 strengths. No pronator drift. Still with visual field defect. GCS 14 (E3V5M6) • HEAD: normocephalic, atraumatic • EYES: PERRLA, conjunctiva clear, sclerae anicteric ,briskly reactive pupils 2-3 mm Bil • NECK: trachea is midline and without any JVD • RESPIRATORY: CTA bilaterally, moving air well, breath sounds symmetric • CARDIOVASCULAR: RRR, normal S1 & S2, no MRG • GI: soft, ND, normal bowel sounds, and non tender • EXTREMITIES: adequate distal perfusion • SKIN: Intact ,Warm,Dry

5. Physical Findings9 Hours Post-Op • NEURO - Lethargic, without any eye opening to stimulation. Grunts to deep sternal rub. Does not follow commands x4 but briskly localizes. Pupils are unequal but briskly reactive, 4mm on the left and 2mm on the right, but GCS 8 (E1V2M5) • HEAD: normocephalic, atraumatic • EYES: PERRLA, conjunctiva clear, sclerae anicteric Briskly reactive pupils 2-3 mm Bil • NECK: trachea is midline and without any JVD • RESPIRATORY: CTA bilaterally, moving air well, breath sounds symmetric • CARDIOVASCULAR: RRR, normal S1 & S2, no MRG • GI: soft, ND, normal bowel sounds, and non tender • EXTREMITIES: adequate distal perfusion • SKIN: Intact ,Warm,Dry

6. Objective Findings

7. Pre-Op MRI

8. Post-Op MRI

9. Hospital Course • Typical hospital course • 1-2 days in the ICU • If no DI can be transferred to the floor and home in another day or two • If develop DI longer stay in the ICU • Patient’s hospital course has been prolonged to an 11 day hospital stay

10. Complications • Severe hypernatremia • Severe dehydration • 10 L free water deficit • Altered level of consciousness • High risk for seizures

11. Pathophysiology

12. Craniopharyngiomas • 2.5-4% of all brain tumors • 80-90% of neoplasms arising in the pituitary region • Tend to arise from anterior superior margin of the pituitary • Some may arise primarily from the 3rd ventricle • Almost all have solid or cystic components • Are not malignant but due to difficulty in curing they are considered “malignant in behavior” • Neurological disturbances, such as headache and visual field defects are initial findings

13. Pituitary Gland

14. Diabetes Insipidus CENTRAL /NEUROGENIC NEPHROGENIC Decrease in the responsiveness of the renal tubule to ADH • Decrease in production of antidiuretic hormone (ADH) or brain edema causes blockage in the pathway from the hypothalamus to the posterior pituitary

15. Causes of Nephrogenic DI • Familial X-linked trait • Pyelonephritis • Renal amyloidosis • Myeloma • Potassium depletion • Sickle cell anemia • Chronic hypercalcemia • Sjogren syndrome • Radiocontrast dye • Drugs • Lithium • Demeclocycline • Amphotericin B • Aminoglycosides • Cisplantin • Rifampin

16. Causes of Central DI PRIMARY SECONDARY TSH Craniopharyngioma Brain Death Tumors Other mass lesions pressing on the hypothalamus – A-comm aneurysms Head injury Primarily basal skull fractures Encephalitis and meningitis Drug induced Ethanol and Dilantin inhibit ADH release • Familial (dominant trait) • Wolfram Syndrome • DIDMOAD

17. Patterns of Central DI • Transient DI • Prolonged DI • Triphasic response

18. Transient and Prolonged DI TRANSIENT DI PROLONGED DI Urine output stays supra-normal for a prolonged time May be supra-normal permanently 33% of these patients will return to normal at 1-year post-op • Supra normal urine output • Polydipsia • Normalizes 12 to 36 hours post-op

19. Triphasic Response • Phase 1: • Injury to the pituitary reduces ADH levels for 4-5 days • Polyuria/Polydipsia • Phase 2: • Cell death liberated ADH for the next 4-5 days leading to transient normalization or even SIADH • Phase 3: • Reduced or absent ADH secretion leading to either transient or prolonged DI

20. Clinical Findings of DI SIGNS AND SYMPTOMS LABORATORY FINDINGS High normal to High serum sodium High serum osmolality Low urine osmolality (specific gravity 1.001 to 1.005) • Polydipsia • 2 to 20 L Daily • Polyuria • > 300 cc/hr for 2 consecutive hours • Dilute urine

21. Pathophysiology

22. Antidiuretic Hormone • Prevents the output of large volumes of urine and can constrict blood vessels to increase blood pressure • Sometimes called “Vasopressin” • Synthesized primarily by neuron cell bodies in the supraoptic nucleus of the hypothalamus • Transported by axons of the hypothalamohypophsial to the posterior pituitary where it is secreted

23. Antidiuretic Hormone • Osmoreceptors synapse with neurosecretory cells in the hypothalamus • Osmoreceptors monitor blood osmolality and blood volume • Increased osmolality stimulates osmoreceptors to leads to secretion of ADH from posterior pituitary • Target tissue is the renal tubules where ADH leads to increased water retention

24. Antidiuretic Hormone

25. Antidiuretic Hormone • ADH attaches to a V2 receptor and activates a cascade through a Gs protein, adenylyl cyclase, cAMP and protein kinase A • Cascade leads to insertion of a aquaporin-2 into the apical membrane of the collecting duct • Water then moves through aquaporin-2 in response to an osmotic gradient and then through aquaporins-3 and -4 in the basolateral membrane and back into circulation

26. Antidiuretic Hormone

27. Vasopressin Receptors

28. Management

29. Managment of DI • Primarily the management of DI in the NCU is handled by Endocrine • At no time should the ICU team order or dose DDAVP • In the short-term if needed may start a vasopressin infusion • In most awake patients their thirst mechanism will prevent them from becoming too dehydrated

30. Management of DI • Desmopressin Acetate • DDAVP • Long-acting synthetic analog of vasopressin • Minimal V1 activity • Antidiuretic-to-pressor ratio is 4000 times that of vasopressin • Half-life is 1.5 to 2.5 hours

31. Management of DI • Vasopressin • Activates both V1 and V2 receptor • Reduces diuresis through increased water permeability and water reabsorption in the collecting ducts • Extrarenal V2 receptors regulate release of coagulation factor VIII and von Willebrand factor

32. Management of DI ARGININE VASOPRESSIN DESMOPRESSIN

33. Questions?