A Case of StudyLyndon Woytuck

Presentation

YA – admitted 12/11/2016 19 years old, male, single, employed in military in janitorial Polyuria of 2 weeks duration

Frequent urination up to once per hour Accompanied by intense thirst and dry mouth Drinking water every hour to compensate for urination Consumed some powder last month to increase muscle mass Weight loss of 3kg in 2 weeks, weight 56kg now Polydipsia, general weakness and abdominal pain

Used to running a time of 11:30min and now 13:40min Diffuse abdominal pain began 2 days prior to admission Gradually worsened until admission, then improved in hospital

No change in urine appearance or odour, no gross haematuria No fever, no nausea, no vomiting, no diarrhoea Background: G6PD, non-modified diet; NKDA

What could it be?

Type 1 DM Monogenic DM (previously MODY) (5% of paediatric cases)

Diabetes is diagnosed within 6 months of birth A strong family history of diabetes is present, without type 2

features (eg, obesity or higher-risk ethnicity) Mild fasting hyperglycemia is observed, especially in young, non-

obese children Diabetes is present, but islet cell autoantibodies, obesity, and

insulin resistance are absent Secondary hyperglycaemia Endocrine tumour Drugs: thiazides, phenytoin, glucocorticoids Pancreatitis When in doubt, treat the patient with insulin and close

monitoring of glucose levels. It is not unusual for adolescents or young adults, particularly Hispanic or African-American patients, to present with DKA and subsequently be found to have type 2 DM

What should be the initial management?

Acute hyperglycaemia is harmful >240mg/dL osmotic diuresis ensues, with loss of glucose, electrolytes,

and water no absolute level of blood glucose elevation mandates admission to

the hospital or administration of insulin in the ED In general, lowering glucose in the ED does not correct underlying

cause and has no long-term effect on the patient’s glucose levels. Volume repletion, insulin therapy, and specific metabolic corrections

are the keys to treatment in DKA and acute hyperglycaemia WBC, blood and urine cultures to rule out infection. Urine ketones are not reliable for diagnosing or monitoring DKA, but

may show if hyperglycemic individual may have a degree of ketonemia.. beta-hydroxybutyrate level—is a more reliable indicator of DKA, with plasma bicarbonate or arterial pH

How much insulin?

The insulin coverage, with a sliding scale for insulin administration Not alone, because it is reactive rather than proactive. The initial daily insulin dose is calculated by patient weight. Usually one

half is administered before breakfast, one fourth before dinner, and one fourth at bedtime. Then adjust the amounts, types, and timing according to the plasma glucose levels so that preprandial plasma glucose is 80-150 mg/dL (4.44-8.33 mmol/L)

Moderate hyperglycemia without ketonuria or acidosis single daily subcutaneous injection of 0.3-0.5 U/kg of intermediate insulin

Hyperglycemia and ketonuria without acidosis or dehydration 0.5-0.7 U/kg of intermediate insulin and SC 0.1 U/kg regular q4-6hr

In HHS, begin a continuous insulin infusion of 0.1 U/kg/h Monitor blood glucose every hour at bedside; if glucose levels are stable for

3 hours, decrease the frequency of testing to every 2 hours Set target blood glucose level at 250-300 mg/dL; adjust downwards after the

patient is stabilized and increase or decrease by 0.5U/h per ∆50mg/dL range Continue intermediate-acting (ie, NPH or Lente) insulin at 50-70% of the

daily dose divided into 2 or, occasionally, 3-4 daily doses. Administer supplemental regular insulin on a sliding scale

Blood glucose should be monitored before meals and at bedtime

Immediate Management

Attended clinic at the military base and referred to ER In ER, blood glucose was found to be >600mg/dL on

fingerstick test and insulin was administered Actrapid 10IU SC and Actrapid 7IU IV and 1000mL 0.9%

NaCl given Metoclopramide 10mg IV KCl administration initiated No blood gas disturbance, acidaemia or ketoacidosis Glycosuria ++++ Ketonuria ++++ Glucose confirmed in serum 722mg/dL

ECG Sinus rhythm and regular Chest X Ray clear and symmetric bilaterally

Diagnosis

Type 1 Diabetes mellitus is characterised by the inability of beta islet cells to produce insulin due to autoimmune destruction

Classic symptoms are Polydipsia, Polyuria, Polyphagia, and Unexplained weight loss

Onset of symptoms may be sudden and may present with DKA

American Diabetic Association Criteria A fasting plasma glucose (FPG) level ≥126 mg/dL (7.0

mmol/L), or A 2-hour plasma glucose level ≥200 mg/dL (11.1

mmol/L) during a 75-g oral glucose tolerance test (OGTT), or

A random plasma glucose ≥200 mg/dL (11.1 mmol/L) in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis

HbA1c assay for diagnosing type 1 diabetes only when the condition is suspected but the classic symptoms are absent.

Why did he present with this episode now?

There is a combined effect of lymphocytic infiltration and destruction of insulin-secreting beta cells of the islets of Langerhans in the pancreas

Cell mass declines, insulin secretion decreases until insulin amount is too small to maintain normal blood glucose levels

After 80-90% of the beta cells are destroyed, hyperglycemia develops

Autoimmunity in genetically susceptible may be triggered by viral infection and production of antigenically similar molecules (eg, enterovirus, mumps, rubella, and coxsackievirus B4)

85% have islet cell antibodies and those directed against glutamic acid decarboxylase (GAD)

Correlated with Grave’s, Hashimoto’s, and Addison’s Approximately 95% of patients with type 1 DM have either

HLA-DR3 or HLA-DR4 polymorphisms

What are the next steps?

Patients need exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism.

Prevent hypoglycaemia due to management errors Prevent or delay microvascular and macrovascular

complications by maintaining good glycaemic control Sensory and autonomic neuropathy Angiopathy Nephropathy Infection Double diabetes

In hospital Management

Hyperglycaemia due to Type I DM (new diagnosis)

Insulin therapy continued Apidra 8U SC once daily (fast) Lantus 16U SC once daily (long)

Investigations Urine output 1000mL overnight HbA1c - 11.0% 13/11 CRP and WBC - normal LFTs - ALP 153 Us and Es - normal Mg 1.80 Glucose 291mg/dL on 13/11 Gluc 283 per urine

What should happen for discharge and follow-up?

Consider patient age for glycemic goals, with different targets for preprandial, bedtime/overnight, and HbA1c levels in patients aged 0-6, 6-12, and 13-19

Benefits of tight glycemic control include continued reductions in the rate of microvascular complications and significant differences in cardiovascular events and overall mortality

Self-monitoring Optimal control requires frequent blood glucose measurement, which

allows rational adjustments in insulin doses. Record blood glucose levels at home and adjust accordingly (CGMs)

Insulin therapy lifelong insulin therapy Usually 2 or more injections of insulin daily basal insulin and a preprandial (premeal) insulin. The basal insulin is

either long-acting (glargine or detemir) or intermediate-acting (NPH). The preprandial insulin is either rapid-acting (lispro, aspart, insulin inhaled, or glulisine) or short-acting (regular).

Diet and activity comprehensive diet plan, with a professional dietitian A daily caloric intake prescription Recommendations for amounts of dietary carbohydrate, fat, and protein Instructions on how to divide calories between meals and snacks Patients should be encouraged to exercise regularly.

Discharge Management

Endocrinological consultation DM diagnosis information and management education Discharge with endocrinological and GP follow-up Use every opportunity to educate the patient and the parents

or caregiver about the disease process, management, goals, and long-term complications

signs and symptoms of hypoglycemia and how to manage it the course of diabetes: they have a chronic condition that

requires lifestyle modification and they are likely to have chronic complications if they do not take control of their disease

Reassure patients about the prognosis with proper management Pay attention to older adolescents who may become detached

from health care A dietitian should provide specific diet control education A nurse should educate the patient about self–insulin injection

and performing fingerstick tests

References MedScape www.Medscape.com UpToDate www.uptodate.com