LOS PELIGROS DEL PRESIDENCIALISMO

Over the years, HHS has been referred to by many names and acronyms. However, it appears that the term HHS has caught on most recently, as it omits the condition of a coma that appeared in previous descriptions. HHS is seen predominantly in type 2 diabetics and is generally defined by the presence of: serum glucose > 33.3 mmol/L, pH>7.3, bicarbonate >15, anion gap <12, serum osmolality >320mOsm/kg, and the absence of serum ketones. The key

distinguishing feature between HHS and DKA is the absence of serum ketones.

Pathophysiology

The pathophysiology of HHS, is very similar to that of DKA. However, the presence of a relatively small amount of endogenous insulin in HHS seems to be a key factor in differentiating it from DKA.

Clinical Presentation

HHS typically evolves over several days to weeks, unlike DKA, which usually begins within a day. Compared to patients with DKA, HHS patients tend to be older, suffer from larger fluid losses, and have more co-morbid illnesses. The mortality has been estimated to approach 15% (nearly 3 times that of DKA). They will usually have less GI symptoms and more recognizable neurological deficits than those patients with DKA. In dealing with these types of patients, it is also important to consider other causes of hyperglycemia, ketosis, and acidosis. In your differential diagnosis, you might also want to consider the possibility of starvation ketosis, alcohol ketosis, DKA, lactic acidosis, and toxic ingestions (i.e. salicylate poisoning, toxic alcohols).

CLINICAL PEARLS

The ‘Big 3’ Aspects of DKA Treatment:

1. Fluid resuscitation

2. Glucose control with Insulin 3. Correction of potassium

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Treatment

The treatment goals of HHS start with correcting the volume and electrolyte losses, and identifying the precipitating causes. Treatment is almost identical to that of DKA. One difference is that there is no role for the use of bicarbonate in HSS. This is intuitive as HHS patients are not likely to be as severely acidotic as their DKA counterparts.

Complications

Patients with HHS usually suffer from multiple co- morbidities and therefore are more susceptible to various vascular and infectious complications. Similar to their DKA cohorts, most of the

complications are iatrogenically related to their fluid and electrolyte replacements. Cerebral edema, ARDS, and coagulopathies remain amongst the most

devastating complications.

HYPOGLYCEMIA

Hypoglycemia is a frequent complication of diabetes, especially in patients requiring insulin. Clinically, hypoglycemia has traditionally been characterized by Whipple‘s Triad:

1. Low plasma glucose

3. Symptoms suggestive of hypoglycemia 4. Prompt resolution of symptoms with

administration of glucose or related product.

Pathophysiology

Normally, as blood glucose falls, insulin secretion is inhibited. In addition, there is an increase in counter regulatory hormones, mainly glucagon and

epinephrine. These hormones stimulate glucose production via gluconeogenesis and glycogenolysis. In order for glucagon to have an effect, the patient must have glycogen stores to mobilize. Patients who are malnourished or alcoholic will likely not have adequate glycogen stores and therefore will not respond to glucagon.

Causes

Most cases of hypoglycemia seen in the ED can be attributed to excessive insulin use in the setting of inadequate oral intake or increased metabolic demands. However, you may also encounter hypoglycemia in the setting of alcohol intoxication, sepsis, liver disease, or the use of oral anti-

hyperglycemics (i.e. sulfonylureas). Rarely, patients will present to the ED with hypoglycemia secondary to insulinomas, hypopituitarism, adrenal

insufficiency, or medication side effects. The key is to suspect the individual cause and treat appropriately.

Symptoms

Symptoms of hypoglycemia can generally be classified as either autonomic or neuroglycopenic. Examples of the latter include headaches, confusion, seizures, and coma. Autonomic or adrenergic symptoms include diaphoresis, nausea, hunger, tachycardia and palpitations. Patients with long standing diabetes occasionally develop a resistance to the signs or symptoms of hypoglycemia with time. This phenomenon is referred to as ‗hypoglycemic unawareness‘. Another important consideration is that patients on beta-blockers will have their adrenergic hypoglycemic symptoms blunted in the setting of hypoglycemia.

Treatment

In the pre-hospital setting, hypoglycemia is often treated by the patients themselves with oral glucose- containing fluids or gels. In the ED, the preferred treatment for adults is IV D50 (dextrose 50%) at 1g per kg, typically starting with 1 ampoule (50g). If the patient does not have an IV, the administration of glucagon 1-2mg sc would be a second line treatment. The downside of glucagon is it takes approximately 10 minutes to work and as mentioned previously, will not be effective in patients without adequate glycogen stores.

In the pediatric population, the treatment of hypoglycemia varies by age (neonates D10 IV at 5- 10ml/kg, infants and children D25 IV at 2-4 ml/kg, adolescents D50 IV at 1-2 ml/kg). It is important to repeat accuchecks every 30 minutes for 2 hours to watch for rebound hypoglycemia. In some situations, a continuous infusion of a dextrose containing fluid will be required.

Disposition

It is important to determine the cause of the hypoglycemia prior to establishing the disposition plan. If hypoglycemia is seen in the setting of a non- diabetic, a thorough workup might need to be pursued. Diabetic patients treated for hypoglycemia who have a quick resolution of symptoms can usually be safely discharged after observation for a few hours. Good diabetic education, assessment /adjustment of their insulin regimen, and adequate follow up with their family doctor or endocrinologist should be arranged prior to discharge. Patients who become hypoglycemic while taking long acting oral hypoglycemics will need a longer observation period.

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SUMMARY

 DKA is a potentially life threatening complication of diabetes. It requires a thorough understanding of physiology in order to provide effective and safe treatment.

 HHS is similar to DKA except that it typically evolves over several days to weeks, there is an absence of serum ketones, and there is a relatively small amount of endogenous insulin. HHS patients tend to be older, suffer from larger fluid losses and other co-morbid illnesses. The mortality is higher with HHS, and there is no role for the use of bicarbonate.

 Patients who present with hypoglycemia require very specific educational discharge instructions.

REFERENCES

1. Charfen MA, Fernandex-Frackelton M. Diabetic ketoacidosis. Emerg Med Clinic N Am 2005; 23:609-628.

2. Soner GD. Hyperosmolar hyperglycemic state. American Family Physician. May 2005; 71(9): 1723-1730.

3. Brodie S. Diabetic ketoacidosis update. Emergency Medicine RAP. December 2004. 4. Trachtenbarg DE. Diabetic ketoacidosis.

American Family Physician. May 2005; 71(9); 1705-1714.

5. Tintinalli J et al, editors. Emergency medicine: A comprehensive study guide. 7th Edition. New York: McGraw Hill. 2011. p1430-1438 and p1440-1444.

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22: ENT Emergencies

Bryan Au

OBJECTIVES

1. To understand the causes, treatment and ongoing care of epistaxis

2. To recognize pharyngitis and understand its treatment options

3. To recognize epiglottitis and appropriately manage it

4. To differentiate between the various deep-space neck infections and appropriately manage them 5. To familiarize yourself with different methods of

foreign body removal from the ears and nose

EPISTAXIS

Introduction

Anterior epistaxis accounts for 90% of all epistaxis. Bleeding most commonly is from Kiesselbach‘s plexus (Little‘s area) on the anterior-inferior nasal septum. Posterior epistaxis, which is more severe, usually originates from the posterior branch of the sphenopalatine artery. The diagnosis of posterior epistaxis is suspected when bleeding is not controlled with anterior packing. Common etiologies of

epistaxis include nasal or facial trauma, digital trauma, low humidity conditions, atherosclerosis, coagulopathy, foreign body, and idiopathic. A careful history will reveal any contributing conditions such bleeding disorders.

Treatment

The ABCs, of course, are paramount. Patients are at risk for aspiration, and should also have a

hemodynamic/volume assessment. Blood work (CBC, INR/PTT, cross & type) and hemodynamic

resuscitation should be done in more severe cases. Any clots should be cleared by blowing the nose or suctioning. The first intervention is to institute proper first aid measures – most people do not know how to stop a nosebleed! Compress the soft, cartilaginous part of the nose for 10-15 minutes (most people incorrectly apply pressure to the nasal bridge). If this fails twice, place an anterior pack. Apply topical anesthesia/vasoconstrictors such as cocaine or lidocaine with epinephrine on soaked pledgets. One may use the traditional layered Vaseline gauze pack, or a commercial nasal tampon or balloon. Once the bleeding has stopped, the patient may be discharged home with the pack in place with instructions to

follow-up in 48-72 hours for re-assessment and pack removal. Anti-staphylococcal antibiotics such as cloxacillin or cephalexin are usually prescribed to prevent sinusitis and toxic-shock syndrome. If the bleeding ceases with anterior pressure, then silver nitrate cautery may be applied to the mucosal bleeding site if it can be identified.

If anterior packing does not control the epistaxis, or if posterior epistaxis is suspected, then obtain ENT consultation. Posterior epistaxis requires admission to hospital for posterior packing with monitoring, and possibly embolization by interventional radiology or arterial ligation.

PHARYNGITIS

Introduction

Pharyngitis is an inflammation/infection of the pharynx and tonsils. Viruses cause the majority of cases (e.g. rhinovirus, adenovirus). The most common bacterial cause is group A streptococcus (GAS). Risk factors for GAS include: winter or early spring, age 5-15 years, and recent exposure to someone with GAS pharyngitis. Strep pharyngitis may rarely result in acute rheumatic fever or post- streptococcal glomerulonephritis.