A 57-year-old-male patient 165 cm tall, and weighing 68 kg in the ASA 1 risk group because of numbness of his left wrist. The biochemical parameters of the patient who was scheduled for operation under regional anesthesia with the diagnosis of carpal tunnel syndrome were as follows; Hb:14.0 mg/dL, Htc:43.0%, Plt:229000/mm3, WBC:6000/mm3, FBG:100 mg/dL, BUN:2817 mg/dL, Creatinine:0.7 mg/dL, AST:20.72 mg/dL, and ALT:12.45 mg/dL. His electrocardiogram (EKC) revealed a HR of 70 bpm with normal sinus rhythm.
Preoperatively the patient was informed about axillary nerve blockade, and his written informed consent was obtained. He didn’t receive any preoperative premedication, and in the operating room, his standard EKG, peripheral O2 saturation (SpO2), and noninvasive blood pressure (NIBP) were monitores. Using a 18 G branule a vein on the back of his left hand was punctured, and 0.09%NaCl infusion at a rate of 200 ml/hr was initiated. Right arm to be operated was positioned at 90° abduction with the torso, and forearm was flexed 90°. After cleansing the surgical field with a sterile antibacterial solution, the site was covered with sterile drape, and a single injection was made with a 22 G x 50 mm needle (Stimuplex® Braun, Melsungen, Germany). Retrograde blood was not observed during negative aspiration.
Using a peripheral nerve stimulator (Stimuplex A; B.Braun Melsungen AG, B.Braun Medical AG CH-6021, Germany) at an intensity of 1.5 mA the nerve was localized. When the intensity of the electrical current was reduced to 0.5 mA, nervous stimuli were observed which made us to think that we were on the innervation site of the nerve to be blocked. Then 40 mL anesthetic solution preprepared by anesthesia technician which we thought to be our routinely used mixture i.e. [20 mL 1% lidocaine (2 ampoules of 2% lidocaine, and 10 mL NaCl 0.09%) and 20 mL 1% prilocaine (10 mL 2% prilocaine, and 10 mL0,09% NaCl)] was injected to the patient with negative suctions after each application of 5 mL. Injection site was compressed for 5 minutes. Nearly 10 minutes later the patient felt numbness on his tongue, irritability, restlessness, agitation, he uttered meaningless words, and moved his arms, and legs senselessly. Decreased peripheral oxygen saturation and presence of peripheral cyanosis led us to make an initial diagnosis of methemoglobinemia, and supportive O2 therapy was initiated via oxygen mask at a rate of 6 lt per minute. We couldn’t measure methemoglobin levels because of lack of necessity facilities. Arterial blood gas measurements were as follows. pH: 7.43 pO2:60.1, and pCO2:44.0. Respiratory distress of the patient increased, and deepened, with a drop in his SpO2 to 76, was intubated under 1 mg/kg propofol, 1 µ/kg fentanyl, and 0.5 mg.kg−1 rocuronium anesthesia to enjure the patency of his airway. For the post-intubation maitenance of anesthesia 50 oxygen –nitrogen, and 1 mac sevoflurane were used. Following induction of anesthesia, hypotension (NIBP: 60/40 mmHg), and bradycardia (HR:40 bpm) developed which required administration of 0.5 mg atropin, and intermittent IV injections of ephedrine (total dose 30 mg). When his health state was stabilized, NIBP values improved, and his HR dropped to 70 bpm with SpO2: 95%, he was amenable for surgery. At the end of the operation which lasted for nearly half an hour, the patient was awakened with injections of 10 µg/kg atropine, and 40 µg/kg neostigmine. Thoughy the patient still continued to articulate meaningless words, and make senseless movements, since he was more cooperative we transferred the patient into the intensive care unit.
When we discerned that in place of 2% lidocaine ampoule which we always requested as a local anesthetic from the pharmacy, 10% lidocaine ampoule was sent, and anesthetic mixture was prepared without checking whether it was 2% lidocaine, we made the diagnosis of local anesthetic intoxication related to wrong formulation of lidocaine rather than methemoglobinemia
During 24-hour monitorization in the intensive care unit his hemodynamic parameters were stable, and his complaints resolved. Then the patient was traansferred to his service with relevant recommendations.
The formula for computing Cockcroft-Gault is given by CrCl = ((140 - age) * adjusted weight * (gender_coefficient)) / (serum creatinine * 72), where the gender_coefficient is 1 if male, and 0.85 if female. The serum creatinine concentration is in mg/dL.
The patient's gender is male, which means that the gender coefficient is 1.
The patient is 57 years old. 
The concentration of creatinine is 0.7 mg/dL. 
The formula for computing the patient's BMI is (weight)/(height * height), where weight is the patient's weight in kg and height is the patient's height in m.
The patient's height is 165.0 cm, which is 165.0 cm * 1 m / 100 cm = 1.65 m. The patient's weight is 68.0 kg. The patient's bmi is therefore 68.0 kg / (1.65 m * 1.65 m) = 24.977 kg/m^2.The patient's BMI is 25.0, indicating they are overweight/obese.
Because the patient is overweight/obese, we use the adjusted body weight formula to get the adjusted weight used for Cockroft-Gault Equation. Shown below is the computation for IBW (ideal body weight).
The patient's gender is Male.
The patient's height is 165.0 cm, which is 165.0 cm * 0.393701 in/cm = 64.961 in. 
For males, the ideal body weight (IBW) is calculated as follows:
IBW = 50 kg + 2.3 kg * (height (in inches) - 60)
Plugging in the values gives us 50 kg + 2.3 kg * (64.961 (in inches) - 60) = 61.41 kg.
Hence, the patient's IBW is 61.41 kg.Shown below is the computation for ABW (adjusted body weight).
To compute the ABW value, apply the following formula: ABW = IBW + 0.4 * (weight (in kg) - IBW (in kg)). ABW = 61.41 kg + 0.4 * (68.0 kg  - 61.41 kg) = 64.046 kg. The patient's adjusted body weight is 64.046 kg.

Using the Cockcroft-Gault equation:
CrCl = ((140 - age) * adjusted weight * gender_coefficient) / (serum creatinine * 72).
Plugging the patient's values gives us ((140 - 57) * 64.046 * 1) / (0.7 * 72) = 105.473 mL/min. Hence, the patient's creatinine clearance is 105.473 mL/min.