Is this patient’s intravascular volume depleted? How would you assess her volume status? What factors would you address in correcting her volume status preoperatively? Which intravenous fluid would you choose?

What metabolic studies are important to evaluate preoperatively? How will this influence your preparation for surgery? Should the case be delayed? If so, why? How long? Is this problem likely to resolve with improvement of her metabolic status? What organ system consequences are there of uncontrolled diabetic ketoacidosis in the acute phase and chronically?

It is very likely that this child has a depleted intravascular volume. Her heart rate is elevated more so than would be due to a low-grade fever. In addition, with fever, insensible losses increase and she has been vomiting. Her blood pressure is low but within normal limits for an 8-year-old girl. Since blood pressure is preserved in hypovolemic children until compensation fails, a “normal” measurement is not reassuring. Dehydration is generally classified according to percentage decrease in body weight. A child who is 3 % dehydrated has a 30 mL/kg deficit and clinically has an increased HR, dry mucous membranes, and concentrated urine. A child with 6 % dehydration has a fluid deficit of 60 mL/kg and a significantly increased HR, very dry mucous membranes, and oliguria. In a child with 9 % dehydration, the fluid deficit is 90 mL/kg, the blood pressure is decreased, and there is poor capillary refill, Kussmaul breathing, and obtundation. Fluid replacement should be with isotonic solution such as normal saline or lactated Ringer’s and should be given relatively rapidly.

Serum electrolytes (Na, K, Cl, HCO₃) and, in addition, phosphorus and calcium, anion gap, glucose, and perhaps blood gases should be evaluated preoperatively [1]. If the child is in diabetic ketoacidosis (DKA), surgery should be delayed at least until intravascular volume has been replenished and control of her DKA is underway. It is entirely possible that her abdominal pain is due to DKA and not any surgical problem [2]. Conversely, acute appendicitis can be the insult that precipitates DKA in a child who has diabetes mellitus but has not yet come to medical attention. While a big part of the problem in DKA is dehydration, overly aggressive replenishment can lead, in some cases, to the development of cerebral edema [3]. Cerebral edema has been documented in many patients during DKA, but most patients remain asymptomatic. Fluid administration should be kept to <4 L/m²/day. In addition, insulin infusion should be tailored to keep the decrease in glucose concentration to 100–180 mg/dL. During therapy for DKA, frequent measurement of serum osmolality is important in preventing a worsening of the cerebral edema.

What are your monitoring considerations? Does this patient need an arterial line? Should the patient have a central venous catheter? A urinary catheter? How would these monitors help your management? Are there any confounding issues?

What agent would you choose to induce general anesthesia? What effects of the various induction methods are particularly important for diabetic patients? For maintenance, which inhalation agent would you choose? Is there a place for a regional anesthetic in this case?

Is succinylcholine safe to give to this patient? What if the pH is 7.25? What is the effect of ketoacidosis on pharmacokinetics of nondepolarizing neuromuscular blockers? Would you administer bicarbonate?

Intra-op ABG: pH = 7.22, PaO₂ = 160 mmHg, PaCO₂ = 34 mmHg, K = 5.5 mEq, Na = 127 mEq, Cl = 97 mEq, glucose = 990 mg/dL.

Standard ASA monitors are indicated, and given the frequency with which serum glucose, electrolytes, and pH will be checked, there is a strong case for adding an arterial line as well. The line will also be very helpful in postoperative management. The case for a central venous catheter is not as strong. If two adequate peripheral IVs and a Foley catheter are in place, she can be managed without a CVP. Urine output will not be a good measure of preload since she will have an osmotic diuresis due to glycosuria. However, the quality of the arterial waveform as well as the improvement of her metabolic acidosis is indicative of the adequacy of her intravascular volume. If there is a question of access or she remains unstable despite what is thought to be adequate fluid replacement, a CVP catheter should be placed after the induction of anesthesia.

The induction of anesthesia should proceed with the assumption that she is not fully fluid resuscitated. This patient should have an intravenous induction. Given her nausea and vomiting, she should have full stomach precautions. Any IV agent can be used if dosed appropriately. Propofol will lead to hypotension if given in the usual doses to a hypovolemic patient. Etomidate will suppress the adrenal cortex in this child with new-onset diabetes mellitus, DKA, and possible appendicitis. The choice of muscle relaxant to facilitate intubation presents difficulties. A nondepolarizing relaxant will take longer to provide intubating conditions in this child who would do better without mask ventilation, while succinylcholine will cause an increase in the serum potassium in a patient who may already have an acidosis-related elevation of serum potassium; it is important to check electrolytes preoperatively.

Succinylcholine can be used but there may be problems. In patients with metabolic acidosis, hypovolemia, and/or hemorrhage, the administration of succinylcholine causes a greater increase in serum potassium that it does in healthy patients. If succinylcholine is used and hyperkalemic arrhythmias occur, treatment with hyperventilation, calcium chloride, and bicarbonate should be started immediately. Nondepolarizing relaxants are also affected by the presence of metabolic acidosis. Metabolic acidosis may augment the neuromuscular blockade from a nondepolarizing relaxant. The antagonism of blockade is not impaired by metabolic acidosis as it is by respiratory acidosis; however, bicarbonate administration should be reserved for severe acidosis (pH <7.2). There are several possible adverse outcomes from bicarbonate administration. Alkalosis will increase potassium entry into cells; bicarbonate may worsen the CNS acidosis. HCO₃ ⁻ combines with H⁺ to form H₂O and CO₂ and CO₂ diffuses rapidly into the CNS while HCO₃ ⁻ does not.

The ABG shows a metabolic acidosis and partial correction with a respiratory alkalosis. The serum glucose is markedly elevated, at 990 mg/dL. The patient’s DKA is not being treated effectively at all. Therapy should include further fluid resuscitation and an additional regular insulin dose of 0.5 U/kg while the insulin infusion continues. The patient has hyponatremia and at the same time hyperosmolality. Serum osmolality can be calculated from the electrolytes as follows:

Should this patient go to the ICU postoperatively? What are you particularly concerned about? How frequently should the patient be metabolically monitored postoperatively?

You are called to the PACU for a urine output of 7 mL in the first 2 h postoperatively. How do you evaluate this? Is a fluid bolus indicated? If so, what type of IV fluid? Is placement of a CVP catheter indicated? Would a urine analysis help understand this situation?

Should this patient’s pain relief be managed with an epidural or morphine PCA? What are the advantages and disadvantages of each?

This patient will be better off in an ICU overnight so that she can have frequent monitoring of her metabolic condition. Even if she had not undergone surgery, her condition was serious enough to warrant an ICU admission. She has arrived with a very large fluid deficit and severe metabolic acidosis. She is at risk for cerebral edema during her resuscitation, and the initial signs of raised ICP might easily be missed if she were not in an ICU. This patient should have hourly determinations of serum glucose, potassium, sodium, pH, and HCO₃. Her urine output, urine ketones, and glucose also should be monitored very often.