Managing Diabetic Keto Acidosis Biology Essay

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Diabetic ketoacidosis (DKA) is a potentially fatal but largely preventable acute metabolic condition. DKA is characteristic of uncontrolled type 1 diabetes mellitus (T1DM) and the incidence of type 1 diabetes mellitus is on the rise in Australia. (Craig, Wong, Alexander, Maguire, & Silink, 2009) According to Wolfsdorf et al. (2007) DKA results from absolute insulin deficiency which is found mainly in undiagnosed T1DM and in patients who neglected to take insulin as required. This paper aims to address the case study of a 21 year old female patient, Megan, presenting with signs and symptoms of DKA. It will relate to relevant aspects of DKA pathophysiology, the initial treatment and the precipitating factors Megan's clinical presentation as outlined in Appendix (A).

In the case study Megan presented to the emergency department with a history of poorly controlled diabetes. The initial assessment of Megan leaves out critical information beneficial to diagnosing and treating DKA. Kitabchi, Miles, Umpierrez, and Fisher (2009) stated the diagnostic criteria for DKA should consist of determining plasma blood glucose levels, blood urea and nitrogen, liver function tests, creatinine, electrolytes, osmolality, serum ketones, urinary ketones, arterial blood gas and full blood count as well as cardiac enzymes with a electrocardiogram. Megan is of childbearing age and a pregnancy screen is warranted. Monitoring of glycosylated haemoglobin may evidence poor glucose control. (Sola et al., 2006) Urine, blood and sputum cultures and lumbar puncture may be beneficial to diagnose infection. A chest x-ray and a thorough history should be taken accompanied by a physical examination. Megan's temperature baseline is vital to monitor for possible infection. Hypothermia due to vasodilation is a poor prognostic sign. (Jerreat, 2010; Kitabchi, et al., 2009; Yehia, Epps, & Golden, 2008) Severity of Megan's DKA may be classified as moderate. The criteria for classification are attached. (Appendix, C)

Megan admitted to consuming a large amount of alcohol over the weekend and possibly neglected her insulin administration. Isidro and Jorge (2010) found that alcohol and drug abuse was a contributing factor in the escalating cost to the state in managing patients with DKA due to concurrent readmissions. With alcohol a major constituent in the case study it is not assumed to be the reason for Megan's presentation. Alcoholic ketoacidosis is characterized by plasma glucose levels that may be mildly elevated to hypoglycaemic according to Kitabchi, et al., (2009) The article suggests that infection and insulin omission are the most common causes of DKA. Insulin omission may be precipitated by psychological factors like eating disorders, fear of weight gain, fear of hypoglycaemia and rebellion. Jerreat (2010) added that error in insulin dosage is common in instigating the initial insulin deficiency as seen with Megan.

Megan's clinical presentation with diarrhoea, abdominal pain, nausea and vomiting is typical to DKA as illustrated by Kearney and Dang (2007). Delayed gastric emptying, ileus, bowel ischaemia and sub acute pancreatitis or esophagitis may be present. Excluding the possibility of these symptoms being a resulting factor from DKA versus a cause of DKA needs to be investigated (Kitabchi, et al., 2009). Jerreat (2010) explains that hyperglycaemia results in glycosuria which raises water and sodium loss leading to dehydration, excessive thirst and abdominal pain. Megan's presentation of abdominal distension is inclusive of these symptoms that closely resemble an acute abdomen. (Wolfsdorf et al., 2007) The presence of ketones induces nausea and vomiting leading to further increases in fluid and electrolyte loss. Potassium, sodium, bicarbonate, magnesium and phosphate are lost. Megan's presentation with premature ventricular beats and sinus tachycardia and weak pulse is a consequence of electrolyte deficiency and severe dehydration. Fluid resuscitation, insulin therapy and potassium replacement should be started simultaneously without delay. (Kitabchi, et al., 2009) Hyperglycaemia leads to increased plasma osmolality and glucosuria due to osmotic diuresis, exacerbating cellular dehydration and electrolyte disturbance further. (Jerreat, 2010) Megan's urine was concentrated depicting established dehydration. Her inability to provide a urine sample alongside her dry, flushed, itchy skin and hypotension is indicative to severe fluid volume deficit. (Jerreat, 2010) Catheterization of Megan's bladder to accurately monitor her output needs to be considered. (Diabetes, 2008)

Megan's blood glucose level is only measured as high and a formal result is not supplied, Megan is assumed to be hyperglycaemic. Kitabchi, et al. (2009) states that increased gluconeogenesis accelerated glycogenolysis and lowered glucose utilisation by peripheral tissue raises the blood glucose level. According to Wolfsdorf et al. (2007), the metabolism of carbohydrates, protein and fat is tightly regulated by insulin in the normal individual. The failure of glucose to enter the cells due to insulin deficiency affects muscle, adipose and liver tissue in the body. Insulin is the metabolic key to transfer glucose from the blood stream into cells. The reduction in effective insulin concentration and the release of counter regulatory hormones lead to further hyperglycaemia and ketosis.

The cause of insufficient insulin can either be absolute or relative, absolute is as a consequence of undiagnosed T1DM or inadequate insulin administration and relative as result from an increased catecholamine release due to stress response. Hyperglycemic crisis patients present with proinflammatory cytokines that are elevated, they include tumour necrosis factor-α, interleukines-(β, -6 and -8).

C- reactive protein, lipid per oxidation, cardiovascular risk factors and plasminogen activator inhibitor-1, these all point to severe inflammation and have been indicated to induce hypercoagulability. Anticoagulation treatment should be considered in Megan's case unless contraindicated. (Kitabchi, et al., 2009) Growth hormone, cortisol and glucagon are released as a result, further increasing the serum glucose level. (Yehia, et al., 2008)

Megan's increase in serum glucose level, the decrease in insulin and the increase in counter regulatory hormones leads to the release of free fatty acids due to lipolysis. (Kitabchi, et al., 2009) Lipolysis is started when the insulin level is too low to inhibit hormone-sensitive lipase (Jerreat, 2010). Ketonemia and Metabolic acidosis is started due to the unrestrained and incomplete fatty acid oxidation in the liver. The abundant ketones responsible are beta-hydroxybutyrate, acetone and acetoacetate. Monitoring of beta-hydroxybutyrate may be beneficial towards establishing the severity of Megan's ketoacidosis (Kitabchi, et al., 2009).

The acid base balance pathology varies depending on the severity of DKA according to Kitabchi, et al., (2009). Megan's arterial blood gas analysis confirms the metabolic acidosis. (Appendix A) Her rapid shallow breathing may be an attempt to compensate the acidic pH of the blood by increasing the release of carbon dioxide and ketones from the lungs. The loss of stomach acids can alter Megan's pH further, possibly masking severe acidosis. The bicarbonate level is markedly decreased this is part of the body's buffering system to neutralise the metabolic acidosis. Due to major osmotic diuresis a large amount of bicarbonate is lost. Altering acidosis with the use of sodium bicarbonate is not recommended; however a minimal amount may be given if pH is below 7.0. Determining the anion gap is useful to establish baseline data towards correcting the acidosis. (Yehia, et al., 2008)

Megan's respiratory rate is 40 and shallow. Kussmaul breathing is expected (Kitabchi, Umpierrez, Murphy, & Kreisberg, 2006) but Megan presents with shallow breaths which is very concerning as this may indicate inability to compensate further and possible inability to maintain her airway. Megan is drowsy and she has impaired cognition which further staves the possibility of central nervous system depression. Kearney and Dang, (2007) contemplated that confusion is a unusual occurrence in DKA and that it is more prevalent in hyperglycaemic hyperosmolar states (HHS) where the serum osmolality is above 340 mmol/L. Central nervous system depression in DKA may quickly lead to coma. A more recent study by Nyenwe, Razavi, Kitabchi, Khan, and Wan, (2010) concluded that acidosis was independently associated with altered sensorium, hyperosmolarity and blood ketone levels were not.

Management of Megan's presentation of DKA should aim at establishing precipitating factors, fluid resuscitation, insulin therapy, correcting metabolic acidosis and electrolyte imbalance (Kitabchi, et al., 2009). Fluid therapy according to Yehia, et al., (2008) should aim to replenish the volume deficit of five to eight litres within the first 24 hours. It's recommended that normal saline should be the first fluid of choice, infused at 15-20 mL/kg/hr, changing to half strength saline if serum sodium level increases. Yehia, et al., (2008) also suggests that the serum osmolality should not decrease by >3 mOsmol/kg H2O/h as it may lead to cerebral oedema. Recommendation in the instance of hypoglycaemia is to change the fluid to 5% glucose or glucose saline once the blood glucose levels decrease < 13 mmol/L (Kitabchi, et al., 2009).

Intravenous Insulin therapy should be initiated according to unit protocol. Care should be taken to replace Megan's potassium to at least > 3, 2 mmol/L (Bull, Douglas, Foster, & Albert, 2007). Yehia, et al., (2008) sited that low dose insulin effectively corrects metabolic acidosis with less complications towards the intra cellular displacement of potassium, the rapid decline in plasma osmolality and plasma glucose. Blood sugar should reduce by 3 - 4 mmol/L per hour. Insulin should be continued until pH, bicarbonate and anion gap normalize. Sub cutaneous insulin therapy should overlap intra venous insulin for one to two hours after resolution of DKA (Bull, et al., 2007).

Megan's potassium should be replaced according to unit protocol. Continuous cardiac and hemodynamic monitoring is essential. Megan should have an arterial line and central venous line placed to accurately and continuously monitor central venous pressure and blood pressure. This will facilitate monitoring and administration of electrolytes. Early detection of deterioration is vital to management of DKA. Megan as with all T1DM should be educated on risk factors and the prevention of DKA. Advice should aim to educate on the early management of concurrent illness and sick day management.

Managing DKA requires a thorough understanding of the pathophysiology of DKA. Initial investigation of presenting signs and symptoms and immediate management of fluid resuscitation, the reversal of acidosis and the replacement of electrolytes should take priority, while continuously monitoring for contributing factors. The incidence of uncontrolled diabetes may be on the rise; however the effective management of DKA is reducing the mortality rate. Resources should be invested in prevention to lighten the economic burden of this preventable condition.

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