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I am a PGY-3 Pediactric resident going into Critical Care/Anesthesia combined fellowship. I serve on our hospital's pediatric/neonatal transport team and had a case yesterday that I wanted to share.
15 yr boy with old PE tubes and chronic suppurative otitis. Private hospital ENT performs tympanoplasty to close the hole, and gives (locally) 10 cc 1:10000 epi intraoperatively. SBP climbs from 120s to 230 instantly, with tachycardia to 160s, clearly intravascular injection. Anesthesiologist pushes 10 mg Labetolol; pressures drop to 90/40s over 20 min. Pt taken to PACU, tachypneic, dyspneic and having frothy hemoptysis. CXR with diffuse bilateral haziness. All told, received 2.5 L LR perioperatively. On our arrival, sitting upright, well-saturated in 6 L O2, which we were able to wean to 4. After 40 mg Lasix, weaned to 2 L and now feeling quite better.
My question regards the pathophysiology. Was this a patient who was relatively volume expanded from the IVFs, whose exogenous cathecolamine bolus made him systemically hypertensive; and then the beta blockade led to the pulmonary edema? Or could the hypertension in itself lead to the edema from changing starling forces? I know this probably is straightforward; I just couldn't get my head around it yesterday. Any insights appreciated.
15 yr boy with old PE tubes and chronic suppurative otitis. Private hospital ENT performs tympanoplasty to close the hole, and gives (locally) 10 cc 1:10000 epi intraoperatively. SBP climbs from 120s to 230 instantly, with tachycardia to 160s, clearly intravascular injection. Anesthesiologist pushes 10 mg Labetolol; pressures drop to 90/40s over 20 min. Pt taken to PACU, tachypneic, dyspneic and having frothy hemoptysis. CXR with diffuse bilateral haziness. All told, received 2.5 L LR perioperatively. On our arrival, sitting upright, well-saturated in 6 L O2, which we were able to wean to 4. After 40 mg Lasix, weaned to 2 L and now feeling quite better.
My question regards the pathophysiology. Was this a patient who was relatively volume expanded from the IVFs, whose exogenous cathecolamine bolus made him systemically hypertensive; and then the beta blockade led to the pulmonary edema? Or could the hypertension in itself lead to the edema from changing starling forces? I know this probably is straightforward; I just couldn't get my head around it yesterday. Any insights appreciated.