1. Review historically the mechanism, incidence, and clinical presentation, followed by a modern reinterpretation, of subdural injection.

2. Summarize published confirmed case reports of subdural injection and outline a new diagnostic algorithm to identify suspected subdural injection.

3. Discuss clinical management of subdural injection.

4. Examine the epidemiology of obesity and its effects on the respiratory, cardiovascular, gastrointestinal, and endocrine systems.

5. Outline anesthesia induction, maintenance, and emergence in the morbidly obese patient.

Unintentional Subdural Injection
Nir Hoftman, MD, Assistant Clinical Professor and Director, Thoracic Anesthesia, Department of Anesthesiology, David Geffen School of Medicine at the University of California, Los Angeles

Historical review of subdural injection: anatomy—small potential space filled with small amount of serous fluid; mechanism—Blomberg (1987) looked at 15 fresh human cadavers; performed continuous lumbar spinaloscopy; questioned existence of subdural space; if existence confirmed, question whether needle could be placed and catheter threaded into subdural space; video trocar inserted through ligamentum flavum into epidural space by loss-of-resistance technique through side port; purposely punctured dura mater into subarachnoid space; then carefully pulled trocar back until able to locate subdural space between layer of arachnoid and dura; easy subdural access in 10 of 15 cadavers, difficult access in 4, and failed access in one; in 6 of 8 cadavers with visible Tuohy needle, catheter easily threaded; incidence—of subdural cannulation 0.82%; percentage comes from retrospective review of >2100 epidurals by Lubenow (1988); subdural block defined as massive neuraxial block without dural puncture; however, no radiologic evidence, only clinical diagnosis; clinical presentation—slow onset (20-40 min); exaggerated (high) sensory block; relative motor sparing; respiratory distress or agitation; cranial nerve findings; mild-to-moderate hypotension; Collier’s indices—moderate hypotension; slow onset of symptoms; slow progression of respiratory incoordination or depression; complete recovery requiring ≥4 hr; Lubenow’s criteria—both major criteria necessary (negative aspiration test and unexpected widespread sensory blockade), plus ≥1 minor criteria (slow onset, variable motor block, or sympatholysis out of proportion to expected epidural blockade)

Modern reinterpretation of subdural injection: anatomy—Reina (2002) looked at 3 fresh human cadavers; imaging performed with electron microscopy; no cadaver had spinal instrumentation; no preimaging manipulation; no anatomic subdural space found; dural anatomy different from previously thought; arachnoid has 2 components, 1) compact laminar layer covering inside of dura, and 2) trabeculated portion, spreading like spider web onto pia mater, coating spinal cord and nerve structure; area between 2 layers called dura-arachnoid interface (composed of cells and amorphous substance); postulated subdural injection caused iatrogenically; found small fissures in dura-arachnoid interface; fissures occurred through amorphous substance; forces and pressure of instrumentation cause traumatic meningeal dissection propagated by further injection; modern incidence—radiology literature on unintentional subdural injection during myelography found incidence of 5% to 13%; however, dura purposely punctured, and sharper needles used; incidence cannot necessarily be extrapolated to anesthesia; however, once subdural injection occurred, when myelography attempted again, second subdural injection would occur; findings mirrored in clinical experience of anesthesia providers; Mehta (1985) studied 100 chronic pain patients; performed epidurals blindly with loss-of-resistance technique; radiologic confirmation of all cases; 7 patients had partial subdural; no clinical correlate; results show that even in expert hands, dura can be punctured and medication can be injected subdurally (or intradurally); Collier (2004) found 11% of blocks subdural

Review of published confirmed case reports

Clinical characteristics: 95% of cases had negative test dose; 89% had negative cerebrospinal fluid (CSF) aspiration (in 11% of cases, could physically withdraw CSF from catheter); all presented with failed block; onset time— overwhelmingly delayed (>10 min; >50% delayed >20 min); one-fifth of cases had fast onset; sensory blockade— 94% of cases had abnormal blockade; most case reports described exaggerated spread; 50% had cranial nerve-type symptoms; one-third of cases had patchy block characteristics; almost one-fifth were restricted; some were unilateral; motor blockade—60% had some type of motor block (favoring lower extremities, although significant amount had motor block in upper extremities); ≈40% did not have any motor block; cardiovascular effects—50% of patients had cardiovascular depression; 4% had full cardiac arrest as presenting sign; 30% had mild hypotension, 17% had severe hypotension, and 13% had bradycardia; respiratory effects—relatively rare; only 25% of patients described respiratory discomfort; severe respiratory problems outnumbered mild respiratory findings; relationship between injectate volume and effect—no correlation between volume injected into subdural space and height of block; however, respiratory depression and motor blockade did correlate with volume

Clinical “flavors”: variable presentations—excessive spread, hypotension, motor block; excessive spread, stable blood pressure (BP), no motor block; CSF aspirated from catheter, delayed onset, restricted block; delayed onset and unilateral block; delayed onset and intractable hypotension; delayed deterioration of normal block

Clinical diagnosis: Collier’s indices not specific enough to make diagnosis; Lubenow’s criteria missed all cases with positive CSF and all cases with restricted spread

New diagnostic algorithm: determine type of neuraxial block (epidural or subarachnoid) present; determine dermatomal distribution (excessive, restricted, or neither); then apply minor criteria (developed based on existing data); limitations—based on radiographically proven cases; only sensitivity can be determined; specificity and positive predictive value cannot yet be determined; reporting bias may skew algorithm, but specificity suspected to be favorable, due to rarity of minor criteria in clinical practice

Clinical management: case—presumed epidural; excessive spread; meets minor criteria of complete cardiovascular stability (uncommon for excessive spread) and complete motor sparing; suggests subdural blockade; imaging shows majority of injection subdural (5 mL); absolutely avoid—withdrawing Tuohy needle from wet tap until CSF ceases to flow, then thread catheter; do not turn Tuohy needle once in epidural space (before threading catheter); consider avoiding (not evidence-based)—epidural after recent lumbar puncture (LP) or wet tap; evidence from study looking at injecting from needle before threading catheter shows fewer paresthesias, fewer intravenous injections, and better blocks; no evidence of increased subdural injection with multiorifice catheter; diagnosis—clinical algorithm; x-ray (posteroanterior [PA] and lateral); computed tomography (CT) with contrast; treatment—supportive care; retry block; use catheter under direct supervision (reports of delayed deterioration); if subdural suspected, do not send patient to hospital floor; consider alternative

Conclusion: subdural presentation highly variable; presenting signs and symptoms may not occur in “classic package”; clinical recognition based on algorithm; definitive diagnosis via imaging (CT with contrast easiest and best); subdural catheters not recommended for clinical use if not in direct presence of patient

Anesthetic Considerations for the Bariatric Patient
Joe C. Hong, MD, Assistant Clinical Professor of Anesthesiology, David Geffen School of Medicine at the University of California, Los Angeles

Classification of obesity: defined by body mass index (BMI); overweight—BMI >25; obese—BMI >30; morbid obesity—BMI >35; extreme morbid obesity—BMI >40

Epidemiology of obesity: 5% of world population (300 million) estimated to have BMI >30; accounted for 15% of US population one decade ago; increased by ≈1% every year; in 2005, incidence of BMI >30, ≈24% (70% of Americans); contributes to ≈$100 billion in health care expenditures each year in United States; contributes to ≈400,000 deaths yearly (quickly approaching smoking as number one preventable risk for death); associated with increased risk for hypertension, diabetes, hyperlipidemia, obstructive sleep apnea (OSA), coronary artery disease, and stroke; risk increases in proportion to BMI; risk greater with android obesity (central distribution of fat)

Respiratory system: physiologic consequences—fat accumulation in thorax decreases chest wall compliance, results in shallow rapid breathing, and increases overall work of breathing; fat accumulation in abdomen pushes diaphragm cephalad, impedes diaphragmatic movement, decreases functional residual capacity (FRC), vital capacity, and total lung capacity; because closing capacity (CC) essentially unchanged, when FRC decreases below CC (eg, when patient supine), shunt formed, causing hypoxemia; OSA—≤70% of obese patients may have OSA; characterized by episodes of apnea lasting >10 sec during sleep; often associated with symptoms of snoring, daytime somnolence, impaired concentration, and memory problems; can lead to obesity hypoventilation syndrome (ie, Pickwickian syndrome); physiologic implications include alveolar hypoventilation, hypoxemia and hypercapnia, secondary polycythemia, pulmonary vasoconstriction and pulmonary hypertension, increased right ventricular (RV) workload, RV hypertrophy, predisposition to RV failure, and increased sensitivity to respiratory depressant effects of inhaled anesthetic agents and narcotics

Cardiovascular system: blood volume—increased total blood volume (2-3 mL per 100 kg of adipose tissue); increased cardiac output (20-30 mL/kg of adipose tissue); decreased blood volume-to-weight ratio (≤50 mL/kg); systemic pressure—increased prevalence of systemic hypertension (up to 50%-60%); generally 3 to 4 mm Hg systolic and 2 mm Hg diastolic increase per 10 kg weight gained; left ventricular hypertrophy (LVH) may result; pulmonary pressure— increased prevalence of pulmonary hypertension; atelectasis results in shunts and hypoxemia; subsequent hypoxic pulmonary vasoconstriction causes increase in pulmonary vascular resistance; cor pulmonale may result; LV function— increased cardiac output due to high BP and increased circulating blood volume; increased LV workload (pressure and volume work), resulting in LV hypertrophy and LV failure; RV function—similar to LV function; RV hypertrophy and RV failure

Gastrointestinal (GI) system: traditional thought (Vaughan 1975) that gastric volume increased and acidity decreased; often have decreased gastric emptying; recommendation to give prokinetics and antacids, rapid-sequence induction, and cricoid pressure; recent studies challenge traditional convention; Harter (1998) found gastric residue not more copious in obese patients; minimal difference in gastric pH; Juvin (2001) confirmed results that gastric volume no different whether patients lean or obese; Maltby (2004) found gastric volumes similar between fasting group and group receiving 300 mL of clear fluids before induction of general anesthesia; gastric pH also did not differ; hepatic function and metabolism—elevated liver function tests (LFTs), increased incidence of fatty infiltration, focal necrosis, and cirrhosis; despite histologic and enzymatic changes, no clear correlation between increased LFTs and hepatic metabolism of anesthetic drugs

Endocrine system: glucose homeostasis—increased resistance of peripheral tissue to insulin; higher prevalence of type 2 diabetes mellitus; predisposes to increased risk for postoperative wound infection and increased risk for myocardial infarction; monitor glucose during perioperative period; exogenous insulin may be required to oppose catabolic response to surgery

Airway: anatomic changes of obesity—cervical and upper thoracic fat pads limit movement of atlantoaxial joint and cervical spine; excessive tissue folds in mouth and pharynx may prevent adequate laryngoscopic view; short, thick neck; obesity not independent risk factor for difficult intubation; Brodsky et al (2002) looking at predictors of difficult intubation found neck circumference, Mallampati classes 3 and 4 airway, history of OSA, male sex, temporomandibular joint (TMJ) pathology, and abnormal upper teeth correlated with difficulty in intubation; BMI alone not correlated with incidence of difficult intubation

Pharmacokinetics: volume of distribution (VD )—total amount of drug in body divided by blood concentration of drug; water-soluble drugs—total body water slightly increased in obesity; small increase in VD for water-soluble drugs; drug requirements close to those for ideal body weight (IBW); fat-soluble drugs—because of increase in adipose tissue, VD markedly increased; drug requirement should be based on total body weight (TBW); Ogunnaike (2002)—propofol induction should be based on IBW, whereas maintenance should be based on TBW; succinylcholine based on TBW rather than IBW because of increased plasma cholinesterase activity in morbid obesity

Induction of anesthesia: ideal technique matter of choice, experience, and confidence in technical ability; take into account—previous anesthetic record, if available; decreased FRC and increased O2 consumption decrease safe apnea time; possible increased risk for pulmonary aspiration; prophylaxis recommended for patients with diabetes or gastroparesis; work-up should include neck circumference, Mallampati classification, and history suggestive of OSA; anticipate difficult airway (need backup equipment and plan); preoxygenate well; position properly; suggested technique— thorough history and physical examination of airway; intravenous (IV) metoclopramide and po sodium citrate; “stacking” maneuver to optimize airway (elevation of head, upper-body, and shoulders above chest to align oral, laryngeal, and pharyngeal axes for good view of vocal cords); surgeon capable of surgical airway readily available; backup equipment; proper oxygenation; cricoid pressure; short-acting IV induction drugs, and succinylcholine; consider awake fiberoptic intubation if airway examination deemed unfavorable

Maintenance of anesthesia

Balanced anesthetic: low solubility inhalation anesthetics—desflurane or sevoflurane; short-acting narcotics—patients with Pickwickian syndrome extremely sensitive to narcotics and inhaled agents; nitrous oxide—high O2 demand limits its use

Avoid intraoperative hypoxemia: avoid spontaneous ventilation; mechanical ventilation with optimal positive end-expiratory pressure (PEEP) to recruit alveoli, increase FRC, and improve lung compliance; pitfalls include reduced preload and hemodynamic collapse; tidal volumes of 10 to 12 mL/kg IBW offers best alveolar recruitment while avoiding barotrauma (tidal volumes >13 mL/kg offer no added advantage)

Emergence: extubate awake in semirecumbent position; supplemental O2 after extubation; continuous positive-airway pressure (CPAP) or bilateral positive-airway pressure (BiPAP) to minimize atelectasis; adequate analgesia to facilitate deep breathing; pulse oximetry and/or arterial blood gases (ABG) as needed to monitor postoperatively

Regional anesthesia: alternative to GA if surgical procedure allows; avoids potential airway difficulties; technically difficult; ultrasonography (US) or nerve stimulator may help guide needle/catheter placement; may require decrease in neuraxial doses by 20% to 25% (due to epidural vascular engorgement and fatty infiltration of epidural space)

Additional considerations: peripheral line placement more difficult; US shown to facilitate placement of central axis blocks and minimize complications; increased risk for compression neurologic injuries, particularly sciatic and ulnar nerves and brachial plexus; case reports of rhabdomyolysis, with incidence of 1.4%; pad gluteal and dorsal muscles against operating room bed