The Glasgow Coma Scale (Score) was developed as a practical structured assessment of consciousness in patients following acute brain trauma. The scale, first described in 1974 and later revised in 1979, scores three different components of responsiveness for a score range of 3 to 15. The levels of response include eye opening (none, to pressure, to speech, spontaneous), verbal response (none, sounds, words, confused, oriented), and best motor response (none, extension, abnormal flexion, normal flexion or withdrawal, localizing, obeying commands), with the worse response receiving the lower number. Generally, scores of 13 to 15 signify mild head injury, 9 to 12 as moderate, and 8 and below as severe. Components of the scale and the overall score seem to strongly correlate to outcome after acute brain injury. A baseline score should be established upon patient presentation, with a revised and more predictive score upon stabilization of respiratory, circulatory, and metabolic abnormalities.

Although the patient suffered acute brain trauma and appears stable, he remains at risk for sudden deterioration secondary to increased hematoma formation or cerebral edema.
Following acute brain trauma, preservation of normal intracranial pressures and mean arterial pressures of more than 70 mm Hg is essential in decreasing poor outcomes. Subdural hematomas are the result of bleeding from bridging veins into the space between the dura and arachnoid. These can develop over the course of a few days and may often result from a seemingly benign injury or spontaneously. Patients will complain of headache and often appear drowsy or obtunded. The diagnosis is via CT scan, and the patient can be managed conservatively or with surgical evacuation. Assuming the patient’s medical condition does not alter over the course of 24 to 48 hours, it would then be safe to proceed with repair of the ankle fracture.

This patient has preexisting paroxysmal atrial fibrillation. Prior to surgery, he should be asked if he knows when his last episode of atrial fibrillation was, if he has symptoms when it is occurring, if he is typically rate controlled, if he was ever on medications for rate control, and if he has ever had a cardioversion or an ablation. Because these patients are more likely to have cardiac disease, a preoperative transthoracic echocardiogram in non-emergent cases is often helpful in evaluating cardiac and valvular functions. Although our patient’s heart rate is controlled, consider the addition of a β-blocker or calcium channel blocker in non-rate-controlled patients, as tolerated by their blood pressure. In addition to inquiring about our patient’s last dabigatran (Pradaxa) use, discuss with the surgical team the plan for possible perioperative anticoagulation.

Often, patients with atrial fibrillation will take an oral anticoagulant to reduce their risk of stroke. Dabigatran etexilate (Pradaxa) is a direct thrombin (factor IIa) inhibitor that is among a group of new oral anticoagulants. Although they are generally easier to manage than warfarin and do not require laboratory monitoring, they do not have specific reversal agents. Thrombin activates factors V, VIII, and IX; helps convert fibrinogen to fibrin; and stimulates platelet aggregation. Dabigatran inhibits both free and clot-bound thrombin. It is a prodrug that is hydrolyzed by serum esterases to its active form. Peak plasma level is within 1.5 to 3 hours of administration, and its half-life is 14 to 17 hours in healthy patients and up to 28 hours in patients with end-stage renal disease. Eighty percent of the medication is excreted unchanged via the kidneys. In patients with normal renal function, the medication should be stopped 24 hours prior to low-risk surgery and 48 hours prior to high-risk surgery. These time intervals are extended up to four times depending on the patient’s renal impairment. In patients not at high risk for thrombosis and with normal creatinine clearance, it may be appropriate to wait four to six half-life intervals from cessation of dabigatran prior to neuraxial injection and removal of epidural catheters.

The Hemoclot direct thrombin inhibitor assay, Ecarin clotting time, and Ecarin chromogenic assay serve as more sensitive quantitative testing for dabigatran activity, whereas a normal activated partial thromboplastin time (aPTT) and thrombin time would suggest lack of significant dabigatran activity. There is no specific reversal agent for excessive bleeding in patients on dabigatran. Recombinant factor VIIa, four-factor prothrombin complex concentrate (PCC), three-factor PCC concentrate, and activated PCC have been suggested for this purpose. A direct dabigatran antibody is under development. In addition, gastric lavage with activated charcoal within 2 hours of administration can be attempted. Ultimately, dialysis will remove the anticoagulant effects of Pradaxa.

An antidote to dabigatran was developed in Germany. This uses the concept of fragment antigen binding (Fab). The drug idarucizumab has already earned the designation of U.S. Food and Drug Administration’s (FDA) “breakthrough” drug and is on fast-track review.

The development of subdural hematoma associated with postdural puncture headache or low CSF pressure is likely similar to development of hematoma following trauma, which is caused by sheering of bridging veins, which are generally at their thinnest point in the subdural space. A review documented 46 cases of subdural hematoma, which developed following intentional dural puncture during spinal procedures or unintentional violation of the dura mater during epidural catheter placement. Given that this patient has already developed a subdural hematoma, neuraxial anesthesia would need to be undertaken with great care, and if done, a spinal should be avoided in favor of an epidural technique.

Neuraxial anesthesia should be considered with caution in this patient with a history of a lumbar fusion at L4-S1. Neuraxial anesthesia can be challenging in this patient population due to abnormalities of the usual landmarks, scar formation, presence of hardware, and bone grafts. These patients are at higher risk for false loss of resistance, inability to access the epidural or subarachnoid space, patchy and failed blocks, unintentional dural puncture, and traumatic needle placement. In a retrospective review of 937 patients with a history of spinal stenosis and/or lumbar disc disease, Hebl et al. showed that prior spinal surgery in 207 of the patients did not affect block success rate or frequency of complications. However, of the 207 patients, only 5 had prior spinal fusion. Care should be taken to confirm that the fusion is at the level that the patient reports. In addition, ultrasound can be helpful in determining the best interspace, correct level, midline, and epidural space depth.

Because this patient does not have any renal insufficiency, the half-life of dabigatran is approximately 14 to 17 hours. After assessing the patient’s current medical status and prior medical history, an anesthetic plan of general, regional, or neuraxial can be considered. If choosing an anesthetic plan of neuraxial anesthesia or one involving deep regional blocks, it is preferable to wait 3 to 4 days, which is 4 to 6 dabigatran half-life intervals. Otherwise, if his atrial fibrillation is stable with preserved cardiac function, and no changes in mental status or deterioration secondary to his subdural hematoma, surgery can proceed within 24 to 48 hours.

Peripheral regional anesthesia for almost all major orthopedic surgery of the lower extremity involves blocking the whole or branches of both the lumbar and the lumbosacral plexuses. In broad terms, the lumbar plexus innervates the ventral aspect of the lower extremity, whereas the sacral plexus innervates the dorsal aspect. The lumbar plexus is made up of the ventral rami of L1-L3, part of L4, and, in 50% of patients, a branch from T12. The plexus is located within the psoas muscle, anterior to the transverse processes of the lumbar vertebra. The plexus gives off the iliohypogastric (T12-L1), ilioinguinal (L1), genitofemoral (L1-L2), lateral femoral cutaneous (L2-L3), femoral (L2-L4), and obturator nerves (L2-L4).

The lumbosacral trunk is formed from ventral rami of L4 and L5 and the anterior branch of S1. The sacral plexus is composed of the union of the lumbosacral trunk with S1-S3 and occasionally S4. The sciatic nerve contains the tibial nerve, which is made up of the anterior divisions of the ventral rami of L4, L5, and S1-S3 and the common peroneal nerve, which is made of the dorsal branches of the same nerve roots. The sciatic nerve splits into the tibial and common peroneal nerves in the popliteal fossa. The common peroneal nerve branches into the superficial and deep tibial nerves. The tibial nerve branches into the medial plantar, calcaneal, and sural (with contribution from communicating superficial peroneal branches) nerves. Other nerves from the lumbosacral plexus include the superior gluteal (L4-S1), inferior gluteal (L5-S2), posterior femoral cutaneous (S1-S3), piriformis (S1-S2), obturator internus (L5, S1-S2), and quadratus femoris (L4-L5, S1).