[PPT] - T2DM and HHS Pathophysiology, differentials, investigations and PowerPoint Presentation

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T2DM and HHS

Endocrinology series

Dr Azeem Alam, MBBS BSc (Hons) Surgical AFP Guy’s and St. Thomas’ Hospital

Content reviewed on the 29/04/2020.

Pathophysiology, differentials, investigations and management.

Cases Quiz

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History A 55-year-old man presents to the GP with lethargy. He mentions that he is always thirsty and has a dry mouth despite drinking ‘gallons’ of water everyday. On examination, he has a large body habitus with a BMI of 32kg/m2. Observations HR 95, BP 152/65 mmHg, RR 20, SpO2 97%, Temp 37.0.

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Case 1

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History A 55-year-old man presents to the GP with lethargy. He mentions that he is always thirsty and has a dry mouth despite drinking ‘gallons’ of water everyday. On examination, he has a large body habitus with a BMI of 32kg/m2. Observations HR 95, BP 152/65 mmHg, RR 20, SpO2 97%, Temp 37.0.

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Case 1

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Pathophysiology

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Pathophysiology

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Pathophysiology

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Pathophysiology

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Pathophysiology

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Definition: a metabolic disorder characterised by hyperglycaemia due to insulin resistance and relative insulin deficiency. Epidemiology

3.5 million people with T2DM in the UK
90% of patients are adults
80% of total cases of diabetes

Risk factors

Age: 45-64 years old
Family history: strong genetic predisposition
Ethnicity
Obesity
Drugs: corticosteroids
PCOS

Pathophysiology

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Pathophysiology

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Clinical features

Symptoms Signs Polyuria Neuropathy

Glove and stocking sensory

loss Polydipsia Retinopathy Polyphagia Diabetic foot disease

Peripheral vascular disease
Calluses
Tissue loss

Weight loss Acanthosis nigricans Fatigue

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Pathophysiology

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Clinical features

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Pathophysiology

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T1DM vs. T2DM

T1DM T2DM Frequency 10-20% 80-90% Pathogenesis Absolute insulin deficiency Insulin resistance Genetics HLA association No HLA association; strong genetic predisposition Presentation Age < 20 years old and

ften acute with DKA

Age > 40 years and gradual onset Acute manifestation DKA Usually HHS Management Insulin Lifestyle à oral medication à insulin

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Pathophysiology

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Primary investigations:

Random blood glucose: ≥ 11.1mmol/L
Fasting blood glucose: ≥ 7.0 mmol/L
Oral glucose tolerance test: ≥ 11.1mmol/L two hours after a 75g oral glucose load
HbA1c: ≥ 48 mmol/mol suggests hyperglycaemia over 3 months

Investigations to consider:

U&Es: screen for renal failure
Urine albumin:creatinine ratio: screen for renal failure
Fasting lipids: screen for dyslipidaemia

Investigations

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Diagnosis

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Management Management

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Pathophysiology

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Glucose

HbA1c: measured every 3-6 months with a target of ≤48 mmol/mol
Self-monitoring: only advised if on insulin

Retinopathy

Immediate ophthalmology referral upon diagnosis and annually thereafter
Arrange urgent review thereafter if:
Acute reduction in acuity
Pre proliferative or proliferative retinopathy
Diabetic maculopathy

Diabetic foot

Should be assessed at least annually; refer urgently to foot protection service if at risk (e.g. ulceration)

Diabetic nephropathy

Annual measurement of eGFR and urinary albumin:creatinine ratio

Monitoring

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Pathophysiology

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Complications

System Complication Cardiovascular

Ischaemic heart disease
Heart failure
PVD

Endocrine

HHS

Neurological

Stroke
Carpal tunnel syndrome
Neuropathy

Renal

Diabetic nephropathy and CKD

Ophthalmology

Diabetic retinopathy
Macular degeneration
Open-angle glaucoma
Cataracts

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Occurs in T2DM
Higher mortality than DKA: 15-20%
Triggers:
Infection
Hypo/hyperthermia
Pancreatitis
Burns
MI/stroke
Medication: ↑ glucose, ↓ insulin or causes dehydration

Hyperosmolar hyperglycaemic state

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Diabetic ketoacidosis

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HHS

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Pathophysiology

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Clinical features

Symptoms Signs Weakness and leg cramps Reduced GCS Confusion, lethargy, hallucinations Dehydration: tachycardia and hypotension Visual disturbance May be confused for a stroke (e.g. hemiparesis) Polyuria Seizures: present in up to 25% of patients Polydipsia Nausea, vomiting and abdominal pain

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Bedside

Urine dip: glycosuria
Bedside ketone and capillary glucose: hyperglycaemia without significant ketonaemia

Bloods

ABG/VBG: hyperglycaemia without a metabolic acidosis
Serum osmolality: estimated using the formula = 2(Na) + urea + glucose
U&Es: electrolyte derangement and AKI due to dehydration
FBC and CRP: raised inflammatory markers may suggest underlying infection

Investigations

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Diagnostic criteria

Joint British Diabetes Societies Inpatient Care Group (2012) Hyperglycaemia: ≥ 30 mmol/L WITHOUT significant hyperketonaemia (< 3 mmol/L) WITHOUT acidosis (pH > 7.3, bicarbonate > 15 mmol/L) Osmolality: usually > 320 mosmol/kg Hypovolaemia

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Management

Fluid resuscitation:

1 litre of normal saline within the first hour
Aim: replace 50% of fluid losses within the first 12 hours

Fixed-rate insulin infusion:

Only started if ketonaemia, or if osmolality is not decreasing with fluids (0.05 U/kg/hour)
Fluid resuscitation alone is usually sufficient
American guidelines differ and state a fixed-rate infusion should be started as for DKA

Other:

Serum osmolality, electrolytes, and glucose should be regularly monitored.
Rapid changes to osmolality must be avoided to prevent central pontine myelinolysis

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Management

Serum potassium concentration (mmol/L) Potassium replacement > 5.5 None 3.5-5.5 40 mmol/L < 3.5 Consider HDU/ITU for replacement via central line

Potassium: patients with HHS are potassium deplete
Anticoagulation: patients are at increased risk of VTE

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Complications

Electrolyte disturbances

Hypokalaemia and hyperkalaemia
Hypophosphataemia and hypomagnesaemia
Hypoglycaemia

Central pontine myelinosis Cerebral oedema

More common in children (70-80% of diabetes-related deaths)
Likely to be iatrogenic

Fluid overload Seizures

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