Topic: Knee arthroscopy - hypertension, tachycardia, pulmonary edema; pheochromocytoma

A 59-year-old 80 kg male presents for left tibial osteotomy.  Four years previously, he received general anesthesia for an arthroscopic menisectomy.  This case occurred prior to the widespread use of pulse oximetry and capnography.

Details of his previous anesthetic: he was premedicated with oral and intravenous diazepam.  He was induced with 360 mg Pentothal, 100 mcg fentanyl, and relaxed with succinylcholine.  He was easily intubated with a 7.5 endotracheal tube.  The initial maintenance was with 2% isoflurane and nitrous oxide.  Initial BP 160/90, HR 84/min.  Isoflurane was discontinued (for unstated reason) 25 minutes after induction.  Anesthesia was then maintained with nitrous oxide, additional Pentothal (450 mg total over the next 25 minutes), and fentanyl (500 mcg over the next 45 minutes).  Just before starting arthroscopy 3 mg pancuronium was given.  Arthroscopy started 30 minutes after induction.  No tourniquet was used.  The surgeon injected 30 cc 0.5% bupivacaine without epinephrine into the joint space.

Ten minutes after starting arthroscopy, BP increased to 220/90, HR 120/min accompanied by bigeminy.  The patient was treated with 2 mg Inderal, 100 mg X 2 iv lidocaine, and 10 mg hydralazine.  The bigeminy resolved, but 10 minutes after the hydralazine the BP increased to 235/110 with HR increasing to 140/minute. Fifteen minutes later the patient was given 40 mg edrophonium (without accompanying anticholinergic), and the HR decreased to 90 – 100/minute with the BP remaining at 210-220/105-110. 

1)  Which of the following are plausible causes of the patient’s tachycardia, bigeminy and severe hypertension?

A)     Light anesthesia in a patient with essential hypertension.

B)     Syringe swap with unintended intravascular injection of epinephrine-containing local anesthetic instead of into the synovial space.

C)  Pheochromocytoma

D)  Severe hypoxemia and hypercarbia in a patient with essential hypertension.

E)  Preoperative use of cocaine or amphetamine overdose.

An ABG was obtained after bigeminy was noted earlier; it showed a moderate mixed acidosis, with pH 7.26 PaCO₂  45 BE –6.9.  K+ = 4.4 mEq/l.  A repeat ABG was obtained 20 minutes after iv hydralazine: pH 7.21 PaCO₂ 37 PaO₂ 75 BE –13.  Nitrous oxide was discontinued.  Pink frothy secretions were suctioned from the endotracheal tube.  40 mg Lasix was given; a Foley catheter was placed draining 400 cc of clear urine.  Esophageal temperature was 35.5^o C. following one hour of systolic BP >200 mm.  Total intravenous fluids were 1 liter D5LR and 800 cc LR.  No muscle rigidity was observed at any time. 

 2)      The absence of muscle rigidity excludes the diagnosis of MH.

A)     True

B)  False

3)      Assume the patient’s minute ventilation was 7 liters/minute.  The absence of respiratory acidosis makes it very unlikely that MH is the underlying diagnosis.

A)  True

B)     False

4)      The absence of temperature rise within one hour of sustained systolic BP >200 mm makes it very unlikely that MH is the diagnosis. 

A)  True

B)  False

The patient remained intubated and was transported to the recovery room.  A nitroglycerin infusion was started at 2.5 mcg/kg/min. and 10 mg iv morphine given.  Four ampoules sodium bicarbonate was given to treat metabolic acidosis.  Blood pressure declined to 160/80, HR 130/minute.  10 mg iv diazepam was given 2 hours into his recovery room stay with an abrupt decrease in BP to 100/60; nitroglycerin was discontinued.  The patient spiked a temperature of 104.5^o F. 8 hours after isoflurane was discontinued.  This was treated with acetaminophen and a cooling blanket.  

The patient’s pulmonary edema and hypertensive crisis resolved without neurologic impairment, and he was extubated the following morning.  His temperature gradually declined over the next 24 hours to less than 100^o F.

Initial CK level in the PACU was normal.  9 hours post-anesthesia the CK = 330, with 8% MB-fraction, consistent with subendocardial myocardial infarction.  17 hours post-anesthesia, the CK level peaked at 4,246 (2% MB-fraction).  Because of the intraoperative metabolic acidosis, postoperative fever and elevated CK level, the diagnosis of MH was considered.  The patient was not referred for diagnostic muscle biopsy.

The patient now presents for a left tibial osteotomy.  Because of the question of MH susceptibility, the anesthesiologist elects to perform a spinal anesthetic accompanied with intravenous sedation. The patient is given 10 mg tetracaine with 0.2 mg epinephrine intrathecally at the L3-L4 interspace.  The patient is sedated with 5 mg iv diazepam and three 50 mg doses of pentothal over 30 minutes.  Initial BP 140/70 with HR 70/minute.  A T8 sensory level is obtained and BP decreases slightly to 125/70 with HR 62.  A thigh tourniquet is inflated at 0810.  Droperidol 1.25 mg iv is given at the same time.  BP increases to 150/85, then further increases to 190/110 with HR 120 at 0850.  The tourniquet is deflated at 0850 with no decrease in BP.  Bigeminy is noted.  The patient complained of substernal chest pain. He is given 100 mg iv lidocaine, 100 mcg X 2 of iv nitroglycerine, and 1” Nitropaste is applied. A left radial arterial catheter was placed.  ABG: PaO₂ 125 PaCO₂ 42 pH 7.34.

5)  The ABG result is consistent with stress-induced MH.

A)     True

B)  False

Temperature was 93^o F.  Surgery was aborted.  The patient was transported to the recovery room.  Hypertension was treated with infusions of nitroprusside and nitroglycerine; esmolol, hydralazine and metoprolol were also given.

After control of the patient’s hypertensive crisis, he was evaluated for presence of pheochromocytoma.  24-hour urine norepinephrine level was >30-fold upper  limit of normal.  Abdominal CT scan confirmed the presence of an adrenal mass. 

Answers:

1.  C, D, E

2.  B

3.  A

4.  A

5.  B

Narrative: 

Undiagnosed pheochromocytoma may present during general or regional anesthesia with hypertension, tachycardia, arrhythmias, sweating, and myocardial ischemia.  Patients with elevated beta-adrenergic tone may have hyperglycemia and tremulousness when awake.  Perioperative hyperthermia and rhabdomyolysis have been reported.  Thyroid storm may present with similar signs, though rhabdomyolysis is rare and extreme hypertension unusual.  Decreased cardiac output and intense vasoconstriction may result in significant metabolic (lactic) acidosis.  MildÛmoderate respiratory acidosis may reflect adrenergic stimulation of carbohydrate and lipid metabolism, or be caused by impaired ventilation from pulmonary edema.  Many of these signs are also present with acute MH, though the unanticipated respiratory acidosis seen with MH is typically worse and much more prominent than may be seen with thyrotoxicosis or pheochromocytoma.  While hypertension and elevated catecholamine levels are frequent observed with acute MH, persistent systolic blood pressure in excess of 200 mm, sudden congestive heart failure, with mildÛmoderate or no respiratory acidosis are much more characteristic of pheochromocytoma than MH.  While not always present, generalized muscle rigidity (that persists despite an intubating dose of non-depolarizing muscle relaxant) is characteristic of MH and some myotonic disorders.   

Noxious stimuli may result in exaggerated hypertension and tachycardia in patients with pheochromocytoma.  Certain medications have been reported to initiate hypertensive crises with pheochromocytoma, including metoclopramide, droperidol, intravascular contrast dye, and histamine-releasing drugs.  Despite releasing histamine, the safe use of atracurium has been reported.  Hyperkalemia is infrequently seen with pheochromocytoma but may result from rhabdomyolysis or increased alpha-adrenergic effect (though the b-2 agonist effect will lower potassium level).

24-hour urine collection for determination of catecholamine levels is highly sensitive for diagnosis.

Numerous medications have been employed in treating hypertensive crisis associated with pheochromocytoma, including nitroprusside, nicardipine, magnesium, nitroglycerine, and phentolamine.  Nitroprusside is a very potent rapid-onset and rapid-offset vasodilator, acting on both venules and arterioles.  Nitroglycerine acts predominantly to increase venous capacitance, but appropriate titration may successfully control hypertension in patients with pheochomocytoma.  Phentolamine is a competitive a-antagonist; it may not be effective if norepinephrine levels are very high; the same limitation applies to the weak a-blockade from labetalol.  Phenoxybenzamine, available only as an oral medication, is given to prepare patients with diagnosed pheochromocytoma for surgery.  Phenoxybenzamine has the advantage of being a non-competitive a-antagonist.  Michael F. James has championed the use of iv magnesium for control of hypertension in pheochromocytoma, in doses similar to those used in treatment of pre-eclampsia, with additional 2 gm boluses given for breakthrough hypertension.  b-antagonists may be added to vasodilator treatment for control of tachycardia, particular in patients with high epinephrine levels.