Clinical Geriatrics

Introduction
Hip fracture is a common, debilitating condition and is increasing in incidence as the population ages. In 1990, there were an estimated 1.7 million hip fractures worldwide, and 90% of these injuries occurred in patients over the age of 50 years. This number is expected to grow to as many as 6.3 million globally by 2050.¹

This case report describes the inherent complexity of providing a safe, continuous spinal anesthetic to a septuagenarian who presented with a host of comorbidities, including acute myocardial infarction (MI) and renal dysfunction, and underwent a surgical repair for hip fracture. Unfortunately, this patient died postoperatively of a cardiac catheterization contrast-induced acute renal insufficiency and respiratory failure. This article reviews literature relevant to perioperative management and anesthesia techniques for this patient population with hip fracture and comorbidities.

Case Presentation
A 73-year-old, 174-pound (79 kg) man fell down while weeding his yard and was taken to an outside medical facility. He was hospitalized with the diagnoses of left femoral neck fracture and acute non-ST segment elevation MI. He had no clear recollection of the events regarding his fall.

The patient’s medical history included: coronary artery disease, for which he had undergone 4-vessel coronary artery bypass grafting nine years prior to this admission; hypertension; a history of living related donor renal transplantation eight years earlier; a history of stroke one year earlier; insulin-dependent diabetes; benign prostatic hypertrophy; and peripheral vascular disease. His medications at home included nitroglycerin 0.4 mg daily, metoprolol 35 mg twice daily, terazosin 5 mg at bedtime, lisinopril 20 mg daily, cyclosporine 125 mg twice daily, prednisone 7.5 mg daily, aspirin/extended-release dipyridamole 2.5 mg twice daily, insulin injection 20 units daily, metformin 400 mg twice daily, finasteride 5 mg daily, amitriptyline 25 mg at bedtime, iron sulfate 325 mg daily, docusate, metoclopramide, and vitamins E and C.

Following admission to the outside hospital, he was initially given two doses of hydromorphone hydrochloride 0.2 mg for pain control. He subsequently became lethargic and hypotensive, with labored breathing. As a result of this constellation of symptoms, the patient was given naloxone 0.4 mg, after which he suffered seizure-like activity. This was terminated with diazepam, and a follow-up computed tomography (CT) scan was negative for any acute intracranial process. Laboratory tests at the outside hospital were remarkable for an elevated troponin I, 18 ng/mL (< 0.04 ng/mL). A Cardiology consult was requested for acute change on the electrocardiogram (EKG) and the increased level of troponin. A transthoracic echocardiogram showed an acute decrease in ejection fraction (EF) of 20-25% as compared to his baseline EF of 40-45%. During his hospitalization at the outside facility, the patient also experienced a marked increase in blood creatinine, increasing from 1.4 mg/dL on hospital day 1 to 3.3 mg/dL on hospital day 4, which continued to deteriorate with oliguria and a urine output of less than 400 mL per day.

Four days after hospitalization and without significant medical improvement, the patient was transferred to a tertiary trauma hospital for definitive care. On admission, he was intubated and sedated with stable vital signs: blood pressure 139/50 mmHg; heart rate 83 bpm; afebrile; and on mechanical ventilation. Laboratory data showed white blood cell count 9.4×10³/µL, hemoglobin 12.7 g/dL, and platelets 145×10³/µL. His chemistry panel was remarkable for elevated blood urea nitrogen (BUN) of 69 mg/dL, blood creatinine of 3.3 mg/dL, and elevated blood glucose of 225 mg/dL. Cardiac enzymes demonstrated a troponin I of 1.46 ng/mL and creatine kinase-MB (CK-MB) of 6.20 units/L.