Post-Tonsillectomy Bleeding

Incidence and Initial Management:

-The incidence of post-tonsillectomy bleeding ranges from 2% to 4%. It is more common in teenagers and young adults than in small children. The vast majority of postoperative bleeding occurs between days 5 and 10 when the eschar separates from the tonsil beds. In rare cases, bleeding may occur in the immediate postoperative period.

-Initial management is tailored to the degree of bleeding. The clot in the tonsillar bed should be suctioned, as spontaneous hemostasis is rare with the clot in place.

-Minimal bleeding may resolve with an ice water gargle or hydrogen peroxide gargle, and older children may tolerate the application of a cautery stick with silver nitrate while awake.

-Administration of antifibrinolytics as tranexamic acid.

-Significant bleeding in a young child, however, typically involves a return to the operating room for a thorough examination of the pharynx and electrocautery hemostasis.

Preoperative Assessment and Optimization:

1-Airway Assessment:

-Although it may be difficult to assess the airway in-depth in an agitated child, observation of the external anatomy and information about airway management from the prior anesthetic should provide sufficient information.

-Even though airway management was uncomplicated previously, it may be more difficult at this time because of postoperative edema and blood-obscuring visualization of the larynx.

2-Intravascular Volume Status:

-It is possible to underestimate the degree of blood loss, since much of it may have been swallowed. Heart rate, blood pressure, and, if possible, orthostatic testing will provide information regarding volume status and guide volume resuscitation.

-Assessing for the presence of tears, moist mucus membranes, skin turgor, and urine output will be helpful as well.

-Adequate IV access, with a large-bore intravenous catheter, should be obtained, if not already present.

-Intraosseous access should be entertained in the hypovolemic, hypotensive patient if IV access cannot be obtained in a timely fashion.

-Volume resuscitation should be initiated with non-glucose-containing isotonic fluids. If the patient is hypotensive, 20 mL/kg boluses of isotonic fluid should be administered until the blood pressure normalizes.

-Transfuse red blood cells if hemodynamically unstable and hematocrit is low.

-Once the bleeding has been controlled and the patient is normovolemic, maintenance fluids should be continued.

3-Laboratory Tests:

-Hematocrit, platelet count, electrolytes, and coagulation studies.

-A specimen should also be sent for serotyping and cross match, as transfusion is a very real possibility.

-Surgery should not be delayed waiting for test results, since bleeding will continue without surgical intervention

Intraoperative Management:

-Management of the airway is of major concern, particularly the ability to visualize the larynx in the presence of ongoing bleeding.

-In preparation for induction, the following should be prepared: multiple laryngoscope blades, a styletted cuffed ETT, and large bore suction.

-The otolaryngologist should be present and tracheostomy equipment immediately available should a surgical airway become necessary.

-The patient is considered to have a full stomach, even if they have not recently eaten, because of swallowed blood.

-A rapid sequence induction is usually performed. However, in the situation where there is significant concern about the airway, a smooth mask inhalation induction with cricoid pressure can be performed with the patient in the right lateral decubitus position with the head down (tonsillectomy position) with suction immediately available. The tonsillectomy position minimizes aspiration risk by promoting the pooling of blood in the oropharynx.

-The choice of IV induction agent will depend on the volume status. Ketamine or etomidate may be used if there is ongoing concern about volume status and hemodynamic stability. Alternatively, propofol may be used but in a decreased dose.

-Muscle relaxation can be achieved with either succinylcholine or rocuronium. However, the duration of action of rocuronium at the dose recommended for rapid sequence induction (1.2 mg/kg) will likely exceed the length of the procedure.

-Volume status should be continually assessed in the face of ongoing bleeding and managed appropriately with isotonic fluids.

-The hematocrit, degree of hemodynamic stability, and status of hemostasis will dictate the need for a blood transfusion.

-Replacement of coagulation factors is rarely necessary. However, if a previously undiagnosed coagulopathy is discovered, the appropriate therapy should be initiated and a hematology consult obtained.

Postoperative Management:

-Patients should be placed in the lateral decubitus position with the head down with supplemental oxygen for transport to the PACU.

-Analgesic and antiemetic medications should be ordered.

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 Multiple Sclerosis

-Multiple sclerosis (MS) is the most common demyelinating neurological disease.

-The myelin surrounding an axon may develop normally and be lost later, but leaving the axon preserved. Alternatively, there may be some defect in the original formation of myelin as a result of an error in metabolism.

-Multiple sclerosis is thought to be autoimmune in nature. Susceptibility to MS may be genetically determined. Viral and immune factors are possibly involved.

-It is characterized by a combination of inflammation, demyelination, and axonal damage in the CNS. Disruption of the blood-brain barrier is an early event. Plaques of demyelination are scattered throughout the nervous system, usually in the optic nerve, brainstem, and spinal cord. The peripheral nerves are not involved.

Preoperative Findings:

1. The commonest presenting symptoms, in order of frequency, are limb weakness, visual disturbances, paresthesia, and incoordination. Legs are more commonly involved before the arms, with signs of spasticity and hyperreflexia. Urinary symptoms may occur.

2. Progression, with remissions and relapses, is very variable. Infection, trauma, and stress may be associated with relapses. A small increase in body temperature can cause a definite deterioration in neural function. The third trimester of pregnancy is associated with a 70% decrease in relapse rate, but this is followed by an increase of about 70% in the first 3 months postpartum. This may impair the ability of a mother to care for her baby.

3. Pain may be a prominent feature, occurring in 45% of patients.

4. Mild dementia and dysarthria may appear as the disease progresses.

5. In advanced disease, and sometimes earlier during acute relapses, respiratory complications may occur secondary to a variety of causes; they were, in decreasing order of importance, respiratory muscle weakness, bulbar weakness, and central control of breathing.

6. MRI now plays an important part in the diagnosis, and abnormalities in the white matter can be seen in 99% of cases. Gadolinium enhancement seems to reflect areas of inflammation where the blood-brain barrier has broken down.

7. Patients are treated with; baclofen, gabapentin, or beta interferon.

Anesthetic Problems:

1. Both experimentally and clinically, an increase in body temperature has been shown to cause a deterioration in nerve conduction and neurological signs.

2. Spinal anesthesia is associated with an increased incidence of neurological complications.

3. Epidural anesthesia in pregnant women with MS showed that there was no difference between those who had been given an epidural and those who had not. Temporary neurological deficits have, however, been reported. It was postulated that neurotoxicity might have resulted from the diffusion of the local anesthetic into the dural space. However, it has been suggested that concentrations of bupivacaine not greater than 0.25% should be used since postpartum relapse has been reported with those above this.

4. Local anesthesia did not significantly increase the relapse rate. However, early disruption of the blood-brain barrier in MS means that local anesthetics can cross more readily, and toxicity is more likely to occur.

5. Neuromuscular blockers. Resistance to atracurium, in association with an abnormally high concentration of skeletal muscle acetylcholine receptors, has been reported in a patient with MS and spastic paraparesis.

6. There is an increased incidence of epilepsy in MS patients.

Anesthetic Management:

1. Elective surgery should not be undertaken in the presence of fever.

2. Spinal anesthesia should probably be avoided. If a regional block is required, epidural anesthesia is preferable.

3. The maximum dose of local anesthetic should be reduced below that normally recommended. Techniques that require large doses should be avoided.

4. It was suggested that IV gamma globulin immediately after delivery protects patients from relapse in the first 6 months postpartum.

5. Patients may require treatment for pain and spasticity.

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Complications of Total Parenteral Nutrition (TPN)

I. Catheter-Related Complications:

-The hyperosmolarity of the dextrose and amino acid solutions requires infusion through large veins or central venous lines.

1-Misdirected Catheter: e.g., with subclavian vein cannulations – (mostly on the right) 10% resulted in misplacement of the catheter in the internal jugular vein.

2-Infection

3-Hematoma

4-Thrombosis

II. Carbohydrate Complications:

1-Hyperglycemia:

-Hyperglycemia is common during TPN; blood glucose levels >300 mg/dl were recorded in 20% of postoperative patients receiving TPN.

-A standard TPN regimen with 1,800 non-protein calories has ≈350 g of glucose, compared to 230 g in a standard tube feeding regimen.

-Tight glycemic control is not recommended in critically ill patients because of the risk of hypoglycemia, which has more serious consequences than hyperglycemia.

-The current recommendation for hospitalized patients is a target range of 140–180 mg% for blood glucose.

2-Insulin:

-If insulin therapy is required, regular insulin is preferred for critically ill patients, to prevent wide swings in glucose levels, by adding insulin to the TPN solutions.

-One shortcoming of IV insulin infusions is the propensity for insulin to adsorb to the plastic tubing in IV infusion sets. This affects the bioavailability of insulin but can be reduced by priming the IV infusion set with an insulin solution (e.g., 20 mL of saline containing 1 unit/mL of regular insulin). But the priming procedure must be repeated each time the IV infusion set is changed.

-SC insulin can be used for stable patients. Regimens will vary in each patient, with a combination of intermediate or long-acting insulin with rapid-acting insulin, when needed.

3-Hypophosphatemia:

-The movement of glucose into cells is associated with a similar movement of phosphate into cells, and this provides phosphate for co-factors (e.g., thiamine pyrophosphate) that participate in glucose metabolism. This intracellular shift of phosphate can result in hypophosphatemia.

4-Hypokalemia:

-Glucose movement into cells is also accompanied by an intracellular shift of potassium (which is the basis for the use of glucose and insulin to treat severe hyperkalemia). This effect is usually transient, but continued glucose loading during TPN can lead to persistent hypokalemia.

5-Hypercapnia:

-Excess carbohydrate intake promotes CO₂ retention in patients with respiratory insufficiency. This was originally attributed to the high respiratory quotient (VCO₂/VO₂) associated with carbohydrate metabolism. However, CO₂ retention is a consequence of overfeeding, and not overfeeding with carbohydrates.

III. Lipid Complications:

-Overfeeding with lipids may contribute to hepatic steatosis.

-Triggering inflammatory response: The lipid emulsions used in TPN regimens are rich in oxidizable lipids, and the oxidation of infused lipids will trigger an inflammatory response. (Oleic acid, one of the lipids in TPN, is a standard method for producing ARDS in animals), and this might explain why lipid infusions are associated with impaired oxygenation.

IV. Hepatobiliary Complications:

1-Hepatic Steatosis:

-Fat accumulation in the liver (hepatic steatosis) is common in patients receiving long-term TPN and is believed to be the result of chronic overfeeding with carbohydrates and lipids. Although this condition is associated with elevated liver enzymes, it may not be a pathological entity.

2-Cholestasis:

-The absence of lipids in the proximal small bowel prevents cholecystokinin-mediated contraction of the gallbladder. This results in bile stasis and the accumulation of sludge in the gallbladder and can lead to acalculous cholecystitis.

V. Bowel Sepsis:

-The absence of nutritional bulk in the GI tract leads to atrophic changes in the bowel mucosa and impairs bowel-associated immunity, and these changes can lead to the systemic spread of enteric pathogens.

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