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Module 10 • Neurology
Neurocritical Care
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Neurocritical Care
Keaton S. Smetana ~2 min read Module 10 of 20
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Neurocritical Care

Table 2. Hyponatremia Clinical Symptoms by Severity of Hyponatremia

Serum Sodium

<120 mEq/L

Serum Sodium

120–130 mEq/L

Serum Sodium

130–135 mEq/L

β€’Headache
β€’Restlessness
β€’Lethargy
β€’Seizures
β€’Brain stem herniation
β€’Respiratory arrest
β€’Death
β€’Malaise
β€’Unsteadiness
β€’Headache
β€’Nausea
β€’Vomiting
β€’Fatigue
β€’Confusion
β€’Anorexia
β€’Muscle cramps
β€’Asymptomatic
β€’Headache
β€’Nausea
β€’Vomiting
β€’Fatigue
β€’Confusion
β€’Anorexia
β€’Muscle cramps
β€’Depressed reflexes
F.

SIADH: Increased secretion of ADH (or vasopressin) results in increased water retention at the renal distal

tubules.

Table 3. Typical Causes of SIADH

Neurologic & Pulmonary Disorders

TBI

Brain tumor

Stroke

Brain infection

Subarachnoid hemorrhage

Intracerebral hemorage

Pneumonia/tuberculosis

Lung cancer

Medications

Desmopressin/vasopressin

Selective serotonin reuptake inhibitors

Tricyclic antidepressants

Carbamazepine

Oxcarbazepine

Chlorpropamide

Cyclophosphamide/iphosphamide

Methylenedioxymethamphetamine

Nicotine

Opioids

Phenothiazine antipsychotic medications

Nonsteroidal anti-inflammatory drugs

MDMA (ecstasy)

MDMA = 3,4-methylenedioxymethamphetamine; TBI = traumatic brain injury.

G.Treatment – Guidelines for diagnosing and managing hyponatremia are available (Intensive Care Med

2014;40:320-31).

Table 4. Treatment Strategies for SIADH

Fluid

Restriction

PO Sodium

IV Sodium

Demeclocycline

Vasopressin

(V)-Antagonists

Mechanism

of action

Restriction

of free water

results in

increased impact

of insensible

losses,

permitting

sodium

concentration to

rise

Sodium

supplementa-

tion

Sodium

supplementation

Inhibition of

ADH activity,

possibly because

of inhibition of

aquaporin water

channels

Inhibition of renal

V2 vasopressin

receptors

(conivaptan V1A

+ V2 receptors;

tolvaptan V2

only)

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