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GR2 - DKA

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jessel tailor

on 19 November 2012

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Transcript of GR2 - DKA

Grand Round 2 Jessel Tailor Miss K.P Demographics: 39 year old unemployed female


PC: Recurrent vomiting, dehydration and abdominal pain


HPC: Symptoms started 3/7 ago and worsening; associated with anorexia, polyuria & polydypsia

Vomiting 'bile'; pain - suprapubic, dull ache, not radiating, or relieved by medication, 7/10

Hasn't been monitoring BM levels for last 'couple of days' but has still been taking insulin

Redeveloping symptoms of a chest infection treated 2 weeks ago with an unknown Abx


PMH: T1DM
Previous episode of DKA when first diagnosed
Asthma
Epilepsy
Depression Ferrous fumarate 305mg OD

Metformin 500mg 1 tablet OM
Metformin 500mg 2 tablets ON
Novorapid 30 units BD
Levemir 25 units ON
Atorvastatin 20mg ON

Salbutomol PRN
Seretide 250 Evohaler BD

Carbamazepine 100mg BD

Mirtazepine 15mg OM

Penicillin allergy with rash FHx: Nil of note

SHx: Lives at home with her father
No alcohol
Ex smoker - 27 pack year history
Independent

Systemic review:
CNS - nil
CV/Resp - nil
Abdominal - 2 year Hx of abdominal distension;
investigated - unknown cause
Urological - nil
Musculoskeletal - nil Examination Obs: BP: 155/65
HR: 122 bpm
Sats: 96% OA
RR: 18 bpm
Temp: 36.2 C

General inspection: Unwell and uncomfortable at rest
SOB, flushed
Alert and oriented in time and place

Cardiovascular: HS I+II+O; JVP normal; no cyanosis or oedema


Respiratory: Chest clear - no added sounds Abdominal: Striae: left and right sides
Dry tongue
Tender: suprapubic, LIF, RIF
No masses/organomegaly
Bladder not distended
BS present

Musculoskeletal: NAD

Neurological: Glasgow coma scale 15/15 Examinations continued What are your differentials? Differential diagnoses Diabetic Ketoacidosis
Acute appendicitis
Sepsis A&E Investigations 1. Urine dip

2. Venous blood gas

3. Bloods - glucose & U&E

4. Sputum sample & CXR

5. ECG ...What are we investigating? Results of note Urine dip: Ketones 5+; glucose 5+; nitrite -ve.

Venous gas: pH 7.26 (~7.32)
pCO2 4.1 kPa (~6.1)
pO2 10.6 kPa (~5.3)
Glucose >41.6 mmol/L
Base excess -11.8 mmol/L (+2 to -2)
HCO3- 15.6 mmol/L (22 - 30)
Lactate 1.9 mmol/L

U&E: Na+ 130 mmol/L (135 - 145)
K+ 4.8 - mmol/L

CXR/Sputum: No consolidation/Nil Plan 1. Bloods - FBC, U&E, glucose, blood culture, amylase

2. Troponin - if raised, start on ACS protocol

3. IV antiemetic

4. Venous gas in 1 hour, then every 2 hours

5. Sliding scale insulin

6. IV 0.9% normal saline (NaCl)
- 1L over 30 mins
- 1L over 1 hour
- 1L over 6 hours + 40mmol KCl Consequent bloods... pH 7.19 (7.26)
pCO2 3.0 (4.1)
pO2 14.5 (10.6)
Na+ 138
K+ 4.0
Glu 9.6 (>41.6)
Lac 9.0 (1.9)

BE -17.9 (-11.8)
HCO3- 10.9 (15.6)

Troponin negative ECG Results Shows T wave inversion in V1, V3, V4, V5, V6
T wave inversion suggests some ischaemic changes Increasing acidosis

Hyperventilating

Insulin initiating glycaemic control



Low bicarb = metabolic acidosis Plan 1. Aggressive fluid management - increase fluid rate

2. Increase insulin infusion rate

3. Repeat ECG if chest pain and do 12 hr trop

4. Hourly obs and venous gas

5. When blood glucose <14 mmol/L, add 125ml/hr 10% dextrose with each additional fluid bag

6. Review for ITU if pH <7.1 Further treatment and updates Venous bloods the next day were normalising but Miss KP refused further blood gasses and IV fluids.

Venous blood: pH 7.34
pCO2 6.5
HCO3- 24.4

With a last BM of 4.6mmol/L, Miss KP self discharged. Diabetic Metabolic
Emergencies
Setting the stage: diabetes
DKA - pathophysiology and management
HHS - an introduction What is DKA Life threatening emergency resulting from insulin deficiency primarily seen in T1DM hyperketonaemia hyperglycaemia Triggers and diagnosis NICE: Confirm the diagnosis (according to local clinical governance) in pts where DKA is suspected and has clinical signs of ketoacidosis:

Nausea and vomiting
Dry skin and mucus membranes
Fruity smell of acetone on the breath
Deep and rapid breathing
Drowsiness or coma Diabetes Mellitus A group of metabolic disorders characterized by chronic hyperglycaemia T1DM
An autoimmune disease in which there is destruction of pancreatic β cells.
Genetic susceptibility and environmental factors T2DM
Decreased insulin secretion and/or peripheral insulin resistance
Associated with obesity, lack of exercise, calorie and alcohol excess T1DM vs T2DM Type 1 Type 2 Epidemiology


Genetics


Cause


Presentation Often before puberty HLA linked Autoimmune β cell
destruction Polydypsia
Polyuria
Weight loss
Ketosis Usually older patients No HLA association Reduced insulin secretion
± insulin resistance Gradual and less severe*
Lethargic
Complications e.g vision *LADA New onset diabetes
Disruption of existing insulin treatment
Infection - commonly pneumonia and UTI NICE targets:
Self: 4.0-7.0 mmol/L pre prandial; <9.0 mmol/L post prandial

Clinical: HbA1c <7.5% (58mmol/mol)/ ≤ 6.5% (48mmol/mol) if increased
arterial risk Management of DKA Diabetes UK: diagnostic criteria 0.9% saline IVI

Fixed rate insulin IVI

Assess obs + investigate

Hourly vital sign regime
SBP <90mmHg: Most - 500ml to 1L 0.9% saline rapidly over 10-15 minutes
Once SBP > 90mmHg, follow below & potassium


SBP >90mmHg: 1L 0.9% saline over next hour


Potassium replacement: In those with K+ <5.5 mmol/L 0 - 60 minutes Fluid regime 1-6 hours Continue fluid replacement -
2h, 2h, 4h


Assess hourly vital signs for reponse to insulin therapy
Falling plasma glucose
Decreasing ketonaemia (OR rising HCO3-)


If ketones or glucose are not falling OR HCO3- not rising
increase insulin infusion in increments of 1 unit/hr
till rates of change are achieved...

Beware of ________ & _______ with increased insulin Blood glucose
Blood ketones (if possible)/ pH Venous HCO3+
Venous K+, electrolytes 6- 12 hours Reduce rate of fluid infusion - e.g. 4h, 6h


Review biochemical and metabolic parameters; review insulin




Check for complications pH
HCO3-
K+
Glucose
Blood ketones if possible BP, JVP, peripheral and pulmonary oedama GCS Infection: ?Antibiotics 10% glucose Continue to
Monitor vital signs
Treat the precipitating cause
Assess any complications

All parameters should be improving/normal

Continue IV fluids if not E+D.


By 24h, ketonaemia and acidosis should be resolved - review fluid & insulin infusion if not
Ketones <0.3mmol/L
Venous pH >7.3 12 to 24 hours Resolution Failure to respond or resolve is unusual and requires
specialist and senior input

Should be eating and drinking normally

Convert to sc insulin when stable and pt is ready to eat

Arrange specialist team input and follow up NICE: Summary and rationale of managing DKA 1. Isotonic saline: replacement of fluid losses

2. Intravenous insulin: correction of hyperglycemia and ketongenesis ( acidosis)

3. K+ replacement: early with frequent monitoring

4. Glucose-containing fluids: if BM <10–15 mmol/L with high rates of insulin infusion

6. Generally avoid use of bicarbonate and phosphate replacement

7. Monitor continuously and review frequently. Hyperosmolar hyperglycaemic state (HHS) DHx: Endogenous insulin, though at reduced levels, is still circulating.

Hepatic ketogenesis is inhibited BUT glucose production still occurs
As a result acidosis is insignificant, or mild (pH >7.3)


NHS: no exact definition exists but UK hospital guidelines suggest:

Hyperglycaemia, often ≥ 30mmol/L
Hyperosmolality, often ≥ 320mosmol/kg
Severely dehydrated and unwell

Osmotic diuresis Hyperosmolar state Hyperglycaemia MI
Stroke
DVT
PE Reduced level of conciousness Pathophysiology and features of HHS Dehydration Arterial or venous thrombosis Hypovolaemia Osmolality in HHS Osmolality is calculated by serum concentrations: = [2Na+] + [glucose] + [urea] Water loss > solutes PLUS hyperglycaemia, results in hypertonic dehydration
[Na+], [Cl-], [HCO3-], [urea], [glucose] all Management aims 1. Treat the cause e.g. antibiotics, diabetes regimen

2. Normalise osmolality + replace fluid and electrolytes

4. Normalise blood glucose

5. Prevent arterial/venous thrombosis complications Osmolality, fluid and electrolytes IV 0.9% saline


IV 0.45% saline



Fluid replacement HHS pts are sensitive to insulin



Insulin in a dehydrated pt will result in cadriovascular collapse:




Commence insulin Insulin regimen Prevent complications


Hyperosmolality and hypernatremia


Altered factor VIII


Contributes to a hypercoagulable state - increased risk of arterial and venous thromboembolism


Prophylactic LMWH in all pts if not CI


Thrombotic complications may be prevented if hypovolaemic correction occurs at To. Use serum osmolality to assess severity and the response to treatment Potassium Add or omit as required based on serum K+ and insulin dosing

Less acidotic means less K+ retention - normokalaemic

If associated pre-renal failure - hyperkalaemia

Pre event diuretics or prolonged vomiting - hypokalaemic Restore circulating volume and rehydrate If fluid balance becomes positive but osmolality does not fall Reduces blood glucose and osmolality



Restores circulating volume and rehydrates Insulin IV not recommended unless significant ketonaemia or ketonuria at To Osmotic shift of water to intracellular space following glucose


Further decline in intravascular volume When blood glucose no longer falling with IV fluids alone Outcomes Mortality from HHS > DKA due to age, co-morbidities and frequency of intercurrent illness in former pts


HHS complete correction will take longer than 24hrs, unlike DKA


All patients require diabetes education to prevent the risk of recurrence and LT complications Thank you! Any questions? Primary impression Diabetic ketoacidosis Longmore et al (2012). Oxford Handbook of Clinical Medicine. 8th Edition. Oxford Univeristy Press, Oxford.
Ballinger, A (2012). Essentials of K&C's Clinical Medicine. 5th Edition. Saunders Elsevier.
Diabetes UK (2012). The management of DKA in adults. Available at: http://www.diabetes.org.uk/Documents/About%20Us/Our%20views/Care%20recs/Joint%20British%20Diabetes%20Societies%20Inpatient%20Care%20Group%20-%20The%20Management%20of%20Diabetic%20Ketoacidosis%20in%20Adults%20-%20Pathway%20Poster.pdf. Accessed on 17/11/12.
NHS Diabetes (2012). Management of the HHS in adults with diabetes. Available from: www.diabetes.nhs.uk/document.php?o=3778. Accessed on 17/11/12.
NICE (2012). Managing type 1 diabetes in adults. Available from: http://pathways.nice.org.uk/pathways/diabetes#path=view%3A/pathways/diabetes/managing-type-1-diabetes-in-adults.xml&content=view-node%3Anodes-managing-diabetic-ketoacidosis. Accessed on 17/11/12
McGuiness, O.P (2005). Defective glucose homeostasis during infection. Annual Review of Nutrition; 25 9-35. Available from: http://www.annualreviews.org/doi/abs/10.1146/annurev.nutr.24.012003.132159. Accessed on 17/11/12
Delany, M. (2000.) DIabetic Ketoacidosis and hyperglycaemic hyperosmolar syndrome. Endocrinology and Metabolism Clinics of North America. Available from: http://www.sciencedirect.com/science/article/pii/S0889852905701596. Accessed on 17/11/12.
NHS Clinical Knowledge Summaries (2011). What is the the pathophysiology of diabetic ketoacidosis. Available from http://www.cks.nhs.uk/diabetes_type_1/background_information/diabetic_ketoacidosis_pathophysiology. Accessed on 17/11/12 References
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