Presentation is loading. Please wait.

Presentation is loading. Please wait.

DI AND SIADH DI AND SIADH Pat Hock RN Pat Hock RN PICU Nurse Educator PICU Nurse Educator Lucile Packard Children’s Lucile Packard Children’s Hospital.

Similar presentations


Presentation on theme: "DI AND SIADH DI AND SIADH Pat Hock RN Pat Hock RN PICU Nurse Educator PICU Nurse Educator Lucile Packard Children’s Lucile Packard Children’s Hospital."— Presentation transcript:

1 DI AND SIADH DI AND SIADH Pat Hock RN Pat Hock RN PICU Nurse Educator PICU Nurse Educator Lucile Packard Children’s Lucile Packard Children’s Hospital Hospital

2 DI and SIADH Disturbances of Water Balance DI and SIADH Disturbances of Water Balance 60% to 80% of the human body is composed of water. 60% to 80% of the human body is composed of water. Water content varies with age, gender, skeletal muscle mass and fat content. Water content varies with age, gender, skeletal muscle mass and fat content. Osmolality is one of several factors regulating fluid balance between the intracellular and extracellular fluid compartments. Osmolality is one of several factors regulating fluid balance between the intracellular and extracellular fluid compartments.

3 ADH: AntiDiuretic Hormone Formed in the supraoptic and paraventricular nuclei of the hypothalamus. Formed in the supraoptic and paraventricular nuclei of the hypothalamus. Transported to the posterior lobe of the Pituitary Gland and stored. Transported to the posterior lobe of the Pituitary Gland and stored. ADH is released: in response to an increase in intravascular osmotic pressure, hypovolemia, decrease in pulse pressure. And in response to fear, pain, anxiety. ADH is released: in response to an increase in intravascular osmotic pressure, hypovolemia, decrease in pulse pressure. And in response to fear, pain, anxiety.

4

5

6 Function of ADH Function of ADH ADH increases the permeability of the renal distal tubule and collecting ducts to water. ADH increases the permeability of the renal distal tubule and collecting ducts to water. Less free water is excreted in urine Less free water is excreted in urine Urine volume is decreased Urine volume is decreased Concentration of urine is increased Concentration of urine is increased

7 Diabetes Insipidus Diabetes Insipidus DI is a clinical condition due to a deficit of ADH or due to the kidney’s resistance to the effects of ADH. DI is a clinical condition due to a deficit of ADH or due to the kidney’s resistance to the effects of ADH. DI may be central (neurogenic) or nephrogenic. DI may be central (neurogenic) or nephrogenic. DI may be a transient or a permanent condition. DI may be a transient or a permanent condition.

8 Etiologies of DI Etiologies of DI CNS disorders that damage or create pressure in the area of the hypothalamus, pituitary stalk, or posterior pituitary gland CNS disorders that damage or create pressure in the area of the hypothalamus, pituitary stalk, or posterior pituitary gland Head Injuries Head Injuries CNS infections CNS infections Intraventricular Hemorrhage Intraventricular Hemorrhage Neurosurgical Procedures: common postoperatively with resection of craniopharyngiomas, pituitary gland tumors, or suprasellar tumors. Neurosurgical Procedures: common postoperatively with resection of craniopharyngiomas, pituitary gland tumors, or suprasellar tumors. Associated with certain drugs: Ethanol, phenytoin, halothane, opiate antagonists, lithium Associated with certain drugs: Ethanol, phenytoin, halothane, opiate antagonists, lithium

9

10 Signs and Symptoms of DI Signs and Symptoms of DI POLYURIA- first sign POLYURIA- first sign Low Urine osmolality (less than 100-200 mOsm/L) Low Urine osmolality (less than 100-200 mOsm/L) Urine specific gravity <1.010 Urine specific gravity <1.010 Hypernatremia (serum sodium greater than 145 mEq/L) Hypernatremia (serum sodium greater than 145 mEq/L) Serum hyperosmolar (greater than 300 mOsm/L) Serum hyperosmolar (greater than 300 mOsm/L) Thirst, polydipsia Thirst, polydipsia Irritability or mental status changes Irritability or mental status changes Dehydration Dehydration Shock Shock

11 Clinical Management of DI Clinical Management of DI Goal is to prevent circulatory failure and hyperosmolar encephalopathy. Goal is to prevent circulatory failure and hyperosmolar encephalopathy. Replace volume deficit and ongoing losses Replace volume deficit and ongoing losses Replace ADH Replace ADH Close monitoring of serum and urine lytes/osmolality Close monitoring of serum and urine lytes/osmolality

12 Fluid Replacement Fluid Replacement Correct Hypernatremia slowly Correct Hypernatremia slowly Bolus with NS if hypotensive Bolus with NS if hypotensive Volume deficit replaced over 24 to 48 hours Volume deficit replaced over 24 to 48 hours Replace ongoing urine losses Replace ongoing urine losses

13 Vasopressin Vasopressin Available IV, subcutaneous, and intranasal forms Available IV, subcutaneous, and intranasal forms DDAVP given intranasally DDAVP given intranasally Pitressin IV Pitressin IV Therapeutic effect: increase in specific gravity and decrease in urine output within 1 hour of dose. Therapeutic effect: increase in specific gravity and decrease in urine output within 1 hour of dose.

14 Nursing Management Nursing Management Close monitoring of intake and output Close monitoring of intake and output Frequent hemodynamic monitoring Frequent hemodynamic monitoring Frequent Neuro assessments Frequent Neuro assessments Serial labs: urine specific gravity and osmolality, Serum sodium and osmolality Serial labs: urine specific gravity and osmolality, Serum sodium and osmolality

15 Complications Complications Cardiac collapse Cardiac collapse Shock Shock Cerebral Edema Cerebral Edema Herniation Herniation Death Death Electrolyte imbalances Electrolyte imbalances Water intoxication and fluid overload Water intoxication and fluid overload

16 Syndrome of Inappropriate AntiDiuretic Hormone Syndrome of Inappropriate AntiDiuretic Hormone SIADH is a clinical condition involving and excess of ADH secretion. SIADH is a clinical condition involving and excess of ADH secretion. The patient is hyponatremic with a low serum osmolality, which normally would inhibit ADH secretion. The patient is hyponatremic with a low serum osmolality, which normally would inhibit ADH secretion.

17 Etiology of SIADH Etiology of SIADH Head Trauma Head Trauma Cerebral Tumors Cerebral Tumors Meningitis Meningitis Cerebral Hemorrhage Cerebral Hemorrhage Pulmonary Diseases Pulmonary Diseases Chronically ill or malnourished children Chronically ill or malnourished children Spinal surgery Spinal surgery BMT or Stem Cell Transplants BMT or Stem Cell Transplants Medications Medications Positive pressure ventilation Positive pressure ventilation

18 Signs and Symptoms of SIADH Signs and Symptoms of SIADH Low urine output in absence of hypovolemia Low urine output in absence of hypovolemia Hyponatremia (serum sodium<135mEq/L) Hyponatremia (serum sodium<135mEq/L) Low Serum osmolality (<285 mOsm/L) Low Serum osmolality (<285 mOsm/L) High urine specific gravity (>1.020) High urine specific gravity (>1.020) Nausea and vomiting Nausea and vomiting Mental status changes Mental status changes

19 Clinical Management Clinical Management Normalize serum sodium over 24 to 48 hours Normalize serum sodium over 24 to 48 hours Normalize serum osmolality Normalize serum osmolality Correct excess extravascular fluid volume Correct excess extravascular fluid volume Prevent neurological sequelae Prevent neurological sequelae Restrict fluids Restrict fluids 3% NaCl 3% NaCl Loop diuretics Loop diuretics

20 Nursing Management Nursing Management Close monitoring of intake and output Close monitoring of intake and output Maintain fluid Restriction Maintain fluid Restriction Frequent Hemodynamic monitoring Frequent Hemodynamic monitoring Frequent Neuro assessments Frequent Neuro assessments Serial labs: serum electrolytes, serum osmolality, specific gravity Serial labs: serum electrolytes, serum osmolality, specific gravity

21 Complications Complications Seizures Seizures Cerebral edema Cerebral edema Cerebral hemorrhage Cerebral hemorrhage Pulmonary edema Pulmonary edema Muscle cramps or weakness Muscle cramps or weakness

22 Triphasic response post Neurosurgery Triphasic response post Neurosurgery Transient DI 12-48 hours postop Transient DI 12-48 hours postop SIADH after transient DI phase lasting up to 10 days postop SIADH after transient DI phase lasting up to 10 days postop Permanent DI Permanent DI

23 Case Scenario #1 Case Scenario #1 A 3 month old is admitted to the PICU for shock with a 2 day history of fever and irritability. Blood and CSF cultures are positive for Streptococcus pneumoniae. He has had decreasing urine output over the last 24 hours (< 0.5 ml/kg/hr)

24 ? Assessment ? Assessment ? Labs might be ordered ? Labs might be ordered

25 Labs Labs Serum Na 126 mEq/L se osmo 260mOsmo/L Na 126 mEq/L se osmo 260mOsmo/L Cl 98 mEq/L Bun 4mg/dl Cl 98 mEq/L Bun 4mg/dl K 3.7 mEq/L Cr 0.4 mg/dl K 3.7 mEq/L Cr 0.4 mg/dl CO2 25mEq/L glucose 129 mg/dl CO2 25mEq/L glucose 129 mg/dl Urine sp gr 1.025

26 ? Abnormal findings ? Abnormal findings ? Etiology ? Etiology ? Treatment ? Treatment

27 Abnormalities Abnormalities Hyponatremia Hyponatremia Oliguria Oliguria Concentrated urine Concentrated urine Low serum osmolality Low serum osmolality

28 SIADH SIADH Treatment: Treatment: Fluid Restriction Fluid Restriction

29 Case Study #2 Case Study #2 A 5 year old (15kg) boy is admitted to the PICU with a history of MVA 2 days ago. He sustained an isolated head injury with an intraventricular hemorrhage and multiple cerebral contusions. Three hours ago he had an episode of severe intracranial hypertension (ICP 90mmHg, MAP 50 mmHg) requiring volume and an epi drip for hypotension. Over the last 2 hours his uo has increased to 130-150 ml/hr (~8ml/kg/hr.) A 5 year old (15kg) boy is admitted to the PICU with a history of MVA 2 days ago. He sustained an isolated head injury with an intraventricular hemorrhage and multiple cerebral contusions. Three hours ago he had an episode of severe intracranial hypertension (ICP 90mmHg, MAP 50 mmHg) requiring volume and an epi drip for hypotension. Over the last 2 hours his uo has increased to 130-150 ml/hr (~8ml/kg/hr.)

30 ? Assessment ? Assessment ? Labs might be ordered ? Labs might be ordered

31 Labs Labs Serum: Na 155mEq/L BUN 13 mg/dl Cl 114 mEq/L Cr 0.6 mg/dl K 4.2 mEq/L glu 86 mg/dl CO2 22 mEq/L se osmo 320 mOsmo/L Urine sp gr 1.005

32 ?Abnormal Findings ?Abnormal Findings ? Etiology ? Etiology ? Treatment ? Treatment

33 Abnormalities Abnormalities Hypernatremia Hypernatremia Polyuria Polyuria Dilute urine Dilute urine High serum osmolality High serum osmolality

34 DI DI Treatment: Treatment: Acute: Vasopressin infusion Chronic: DDAVP Monitor for Hyponatremia

35 References References Curley, Critical Care Nursing of Infants and Children. Saunders Curley, Critical Care Nursing of Infants and Children. Saunders Hazinski. Manuel of Pediatric Critical Care. Mosby Hazinski. Manuel of Pediatric Critical Care. Mosby Kliegman. Nelson’s Textbook of Pediatrics. Saunders Kliegman. Nelson’s Textbook of Pediatrics. Saunders Slota. AACN’s Core Curriculum for Pediatric Critical Care. Saunders Slota. AACN’s Core Curriculum for Pediatric Critical Care. Saunders


Download ppt "DI AND SIADH DI AND SIADH Pat Hock RN Pat Hock RN PICU Nurse Educator PICU Nurse Educator Lucile Packard Children’s Lucile Packard Children’s Hospital."

Similar presentations


Ads by Google