Titis Kurniawan

Fakultas Ilmu Keperawatan

Universitas Padjadjaran

Outline

� Physiology of ADH

� Hyponatremia

� SIADH & Etiology� SIADH & Etiology

� Diagnostic test

� Sign & Symptom SIADH

� Patofisiology SIADH

� SIADH Management

Anti Diuretic Hormone� Kelenjar pituitary posterior menghasilkan ADH & oxitosin

� Disekresi dari kelenjar pituitary posterior sbg respon terhadap:

� Peningkatan onkotik plasma

� Peregangan atrium kiri

� Olahraga� Olahraga

� Keadaan emosional tertentu

� Bekerja pd duktus kolektivus ginjal� M>> absorbsi air

� Kekurangan ADH (Diabetes insipidus) � absorbsi air di tubulus

ginjal << � hipernatremia, poliuria & BJ urine rendah

� Kelebihan sekresi ADH (SIADH) � absorbsi air di tubulus ginjal

>> � Dilutional Hyponatremia, oliguria, & BJ urine tinggi

Hyponatremia� Sign & symptoms:

� Cells swelling

� Cerebral edema; Seizure, headache, confusion, unconsciousness/coma

� Restlessness

� Muscle weakness� Muscle weakness

� Muscle spasm/cram

� Nausea/vomiting

� Caused by SIADH and other causes

� Mortality rate in hyponatremic patients 50x higher than non

� Mortality rate in patients with Na serum < 120 � twice those

� Mortality in adult patients (5-50%) >> infant (8%)

SIADH� Adalah: Kondisi dimana ADH disekresikan secara berlebihan dari kelenjarpituitari posterior� retensi air � intoksikasi air (hipoosmolality serum & hyponatremia)

� Kriteria Diagnostik:

1. Hypo-osmolality; plasma osmolality > 280 mosmol/kg, or plasma sodium concentration < 134 mmol/lconcentration < 134 mmol/l

2. Inappropriate urinary concentration (Uosm >100 mosmol/kg) forhyponatraemia

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

Laboratory Test

� Electrolyte test; Na, K

� Serum & urine osmolality;

� Serum osmolality <<

� Urine osmolality >>, high serum Na (> 30 � Urine osmolality >>, high serum Na (> 30

mosm/L)

�BUN � urea <<

�Other laboratory test; blood glucose

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 injuryhemorrhage, 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

Malignancy

Drug

Pulmonary infection

Cerebral edema

GIT

Headhace, seizure, Coma,

unconsciousness, TTIK,

irritable, confusion

Nausea, Vomiting, Abdominal

cramp, anorexia, thirst

PatofisiologyWater intoxicacy

HyponatremiaWater retention

Cells edema

Hypoosmolarextra celular

Cardiovascular CVP>>, TD>>

Musculosceletal Weakness,

fatigue, muscle

crampUrinaria

Oliguria, BJ urine <<

Manifestasi Klinis SIADH

� Plasma sodium (> 130 mmol/L) Asymptomatic

� Plasma Sodium (125 – 130 mmol/L); anorexia, nausea, vomiting, &

abdominal pain/cramp

� Plasma Sodium (115 – 125 mmol/L); >> TD, >> BB, headache,

agitation, confusioon, hallucination, incontinence, & other 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� asymptomatic

Serum Values of Electrolytes

Cations Concentration, mEq/L

Sodium 135 - 145

Potassium 3.5 - 4.5

Calcium 4.0 - 5.5Calcium 4.0 - 5.5

Magnesium 1.5 - 2.5

Anions

Chloride 95 - 105

CO2 24 - 30

Phosphate 2.5 - 4.5

Medical 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 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

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� 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� 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.neurological symptoms.

� Results from overcorrection of sodium

� Correction of > 25 mEq per 24-48 hrs

� Concurrent hypoxia

� Presence of liver disease

� Acute correction limit 25 mEq /day

� Chronic correction limit 10 mEq/day