04/05/2013

Syndrome Inappropriate ADH

(SIADH)

Titis Kurniawan, MNS

Outline
Physiology of ADH Hyponatremia SIADH & Etiology Diagnostic test Sign & Symptom SIADH Patofisiology SIADH SIADH Management

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Physiology of Anti Diuretic Hormone (ADH)

Pituitary gland;
Posterior menghasilkan ADH & oxitosin Anterior; growth hormone, LH, FSH

ADH released when:

Osmolality serum >> Exercise Dehidration

Work on ductus colektivus renal >> water absorbtion << ADH << water absorbtion in ductus collectivus renal hypernatremia, poliuria & low urine osmolality Diabetes Insipidus >> ADH (SIADH) >> water aborbtion in ductus colectivus renal >> Dilutional Hyponatremia, oliguria, & high urine osmolality

Physiology of ADH

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Hyponatremia
Normal range; 135 145 mmol/L Sign & symptoms:
Cells swelling Cerebral edema; Seizure, headache, confusion, unconsciousness/coma Restlessness Muscle weakness Muscle spasm/cram Nausea/vomiting

Caused by SIADH and other causes Mortality rate 50x higher than nonhyponaremia & increased twice Na serum < 120. Adult patients (5-50%) >> infant (8%)

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SIADH
Is: condition where ADH hypersecreted from posterior pituitari gland >> retensi water retention/intoksikasi air (hipoosmolality serum & hyponatremia) Diagnostic Criteria: 1. Hypo-osmolality; plasma osmolality <280 mosmol/kg, or plasma sodium concentration < 134 mmol/l 2. Inappropriate urinary concentration (Uosm >100 mosmol/kg) for hyponatraemia 3. Elevated urinary sodium (> 40 mmol/l), with normal dietary salt and water intake 4. Patient is clinically euvolaemic 5. Exclusion of hypothyroidism, diuretics and glucocorticoid deficiency particularly in patients with neurosurgical conditions

.....SIADH
Laboratory test;
Electrolyte test;
Na; < 134 mmol/L

Serum & urine osmolality;

Serum osmolality <<(Normal 278 300 mOsm/Kg) Urine osmolality >> Natrium urine >>

BUN urea << (Normal = 7-18 mg/dL) Other laboratory test; blood glucose (fasting Normal ; 70-110 mg%)

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Etiology of SIADH
Malignancy; small cell lung cancer, nasopharyngeal cancer, mesothelioma, GI tract malignancy, Lymphoma, sarcoma. CNS Disorder/Intracranial Diseases; tumor, meningitis, encephalitis, abscess, subarachnoid hemorrhage, subdural hemorrhage, traumatic brain injury Medication; desmopressin, selective serotonin reuptake inhibitors (SSRI, carbamazepine, haloperidol, quinolones, vincristine, etc), narcotic, general anesthesia, thiazide diuretic, hypoglycemic agent Pulmonary; pneumonia, TB, vasculitis, Positive pressure ventilation

Patophysiology
Cerebral edema Headache, seizure, confusion, ICP >>, coma Nausea, Vomiting, Abdominal cramp, anorexia, thirst
CVP= Normal/high, TD relatif Normal

GIT

Cardiovascular

Cell edema
Hypoosmolar extracellular

Musculosceletal

Weakness , fatigue, muscle cramp

Urinary Water Excess

Hyponatremia

Oliguria, BJ urine >>, Na urine >>

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Sign & Symptoms

Plasma sodium (> 130 mmol/L) Asymptomatic Plasma Sodium (125 130 mmol/L); anorexia, nausea, vomiting, & abdominal pain/cramp Plasma Sodium (115 125 mmol/L); headache, agitation, confusioon, hallucination, incontinence, & other neurological symptoms Hyponatremia < 115 mmol/L; pulmonary edema, neurological squele, seizure & coma due to >> Intracranial pressure Patient with intracranial problem (space-occupaying lesion & neurosurgical treatment), the onset of symptom my occur at higher level of sodium concentration In chronic hyponatremia mechanism) asymptomatic (addaptation

SIADH Management
Fluid restriction (7-10ml/KgBB/Day) depend on hyponatremia severity lower serum level more aggressive restriction Gradual correction of sodium serum level with IV electrolyte, food, fluids. Medication; demecocycline/lithium (block ADH) Identified underlying causes of SIADH and provide recommended therapy (surgery, radiation, antibiotic) Drugs suspected as SIADH etiology must be STOPED

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Nursing Management
Assessment:
History; medication, malignancy, lung infection, etc Hydration: skin turgor, I:O, daily weight, vital sign (TD, RR, HR, etc), CVP, urine characteristic etc Cells edema signs & symptoms; neurological status, GIT, etc

Diagnosis:
Excess fluid volume Electrolyte imbalance Disturbed thought process

Intervention
Monitoring I/O (including educating family in recording I/O & BW) Monitoring neurological status; take seizure precautions Work with patients & family to run fluid restriction Encouraged high sodium fluids (tomato juice, milk) Sugar less gum for minimizing dry mouth during fluid restriction Therapy of underlying causes of SIADH

Central Pontine Myelinosis

Is; Neurological disease caused by severe damage of the myelin sheath of nerve cells in the brainstem Characterized by acute paralysis, dysphagia (difficulty swallowing), and dysarthria (difficulty speaking), and other neurological symptoms sometimes presence of liver disease & concurent Hypoxemia Resulted from overcorrection of sodium
Correction of > 25 mEq per 24-48 hrs Acute correction limit 25 mEq /day Chronic correction limit 10 mEq/day