Somatostatin analog

Octreotide (Sandostatin)

Also called Sandostatin

Reviewed by Alex G, BSN, RN, CEN, CCRN, CMC, NREMT-P · From the Reference tab of the app

Indications

Acute variceal bleeding, started on suspicion and continued 2–5 days with band ligation and antibiotics (off-label)
Carcinoid crisis and carcinoid syndrome flushing and diarrhea, including during anesthesia
Recurrent hypoglycemia after sulfonylurea overdose (off-label)
High-output fistula, chylothorax or secretory diarrhea (off-label)
Hepatorenal syndrome with midodrine and albumin when terlipressin or norepinephrine cannot be used (off-label)
GI bleeding from angiodysplasia, including in LVAD patients (off-label)

Dosing

Octreotide drip card and mL/h converterStart: 50 mcg bolus, then 50 mcg/h

Mechanism of action

Octreotide, an 8-amino-acid analog of the 14-amino-acid hormone somatostatin, binds somatostatin receptors, mainly SSTR2 and SSTR5. These Gi/o-coupled receptors inhibit adenylyl cyclase, open potassium channels and close calcium channels, so cells release less growth hormone, insulin, glucagon, TSH, gastrin, VIP and serotonin. Suppressing glucagon and other vasodilator peptides constricts splanchnic arterioles and cuts portal inflow, but each bolus lowered portal pressure for only about 5 min, an infusion did not sustain it, and repeat boluses worked less (Escorsell 2001).

Pharmacology

GI: lowers splanchnic and portal flow; slows motility; cuts pancreatic and intestinal secretion and fistula output
Endocrine: inhibits growth hormone, glucagon and insulin more potently than somatostatin; glucose can rise or fall
Cardiovascular: bradycardia (under 50/min in 25% of acromegaly patients) and conduction delay (label); MAP rises briefly after a bolus
Hepatobiliary: inhibits gallbladder contraction, so sludge and stones form with prolonged use
Other: suppresses TSH; reduces fat absorption and vitamin B12

Pharmacokinetics

Onset	IV: immediate; SC: peak level in about 25 min
Duration	Hormone suppression up to 12 h after an SC dose (label); the portal effect of a bolus lasts minutes
Half-life	1.7–1.9 h, against 1–3 min for native somatostatin (label)
Distribution	Vd 13.6 L (about 0.2 L/kg), largely extracellular
Protein binding	About 65%, mainly to lipoproteins
Clearance	7–10 L/h; about 4.5 L/h in dialysis-dependent renal failure (label)
Elimination	About 32% unchanged in urine; the rest mostly hepatic
Organ failure	Cirrhosis: half-life 3.7 h; older adults: half-life 46% longer (label)
Routes	IV bolus and infusion or SC (bioequivalent); monthly IM depot for chronic disease

Chemistry

Cyclic octapeptide D-Phe-Cys-Phe-D-Trp-Lys-Thr-Cys-Thr-ol with a disulfide bridge (MW 1,019)
Keeps somatostatin's Phe-Trp-Lys-Thr binding turn; the D-amino acids, ring and C-terminal threoninol block peptidases, stretching the half-life from minutes to nearly 2 h
Water-soluble acetate salt in vials of 50–1,000 mcg/mL; multiple-dose vials contain phenol; refrigerate (14 days at room temperature, protected from light)
Stable 24 h in NS or D5W; incompatible with TPN (label)

Adverse effects and cautions

In the one-pagers

LVAD BasicsComplications: bleeding, stroke, infection, RV failure: Hold warfarin (and aspirin in HeartMate II or HVAD patients), reverse only for life-threatening bleeding with a high INR, and scope early. For recurrent bleeding ISHLT 2023 lists a lower INR target, octreotide and thalidomide as options with thin evidence.

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Sources

FDA label: Sandostatin (2024)
Escorsell 2001 (octreotide desensitization)
Baveno VII consensus (2022)

For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow your local protocols and medical direction.