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    Hyperosmolar Hyperglycaemic State

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    jsdlzj
    Hyperosmolar hyperglycaemic state (HHS) is characterized by extreme hyperglycemia, hyperosmolality, and absence of ketoacidosis. It is often precipitated by infection, acute illness, surgery, medications, or endocrine disorders in elderly or uncontrolled diabetic patients. Patients present with dehydration, altered mental status, and sometimes seizures. Treatment involves fluid replacement, insulin administration, and treating the underlying cause. HHS has higher mortality than diabetic ketoacidosis, especially in patients over 70 years old, due to risks of complications like venous thromboembolism and cerebral edema.

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    Hyperosmolar Hyperglycaemic State

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    jsdlzj
    32 views3 pages
    Hyperosmolar hyperglycaemic state (HHS) is characterized by extreme hyperglycemia, hyperosmolality, and absence of ketoacidosis. It is often precipitated by infection, acute illness, surgery, medications, or endocrine disorders in elderly or uncontrolled diabetic patients. Patients present with dehydration, altered mental status, and sometimes seizures. Treatment involves fluid replacement, insulin administration, and treating the underlying cause. HHS has higher mortality than diabetic ketoacidosis, especially in patients over 70 years old, due to risks of complications like venous thromboembolism and cerebral edema.

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    Hyperosmolar Hyperglycaemic State

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    Hyperosmolar hyperglycaemic state (HHS) is characterized by extreme hyperglycemia, hyperosmolality, and absence of ketoacidosis. It is often precipitated by infection, acute illness, surgery, medications, or endocrine disorders in elderly or uncontrolled diabetic patients. Patients present with dehydration, altered mental status, and sometimes seizures. Treatment involves fluid replacement, insulin administration, and treating the underlying cause. HHS has higher mortality than diabetic ketoacidosis, especially in patients over 70 years old, due to risks of complications like venous thromboembolism and cerebral edema.

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    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    32 views3 pages

    Hyperosmolar Hyperglycaemic State

    Uploaded by

    jsdlzj
    Hyperosmolar hyperglycaemic state (HHS) is characterized by extreme hyperglycemia, hyperosmolality, and absence of ketoacidosis. It is often precipitated by infection, acute illness, surgery, medications, or endocrine disorders in elderly or uncontrolled diabetic patients. Patients present with dehydration, altered mental status, and sometimes seizures. Treatment involves fluid replacement, insulin administration, and treating the underlying cause. HHS has higher mortality than diabetic ketoacidosis, especially in patients over 70 years old, due to risks of complications like venous thromboembolism and cerebral edema.

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    © All Rights Reserved
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    Hyperosmolar hyperglycaemic state

    Definition
     Non-ketotic hyperglycaemic syndrome
     Defined as extreme elevation in serum glucose (BSL >33.3) + hyperosmolality (>320mmol/kg) and
    absence of ketoacidosis (pH >7.3 + HCO3 >15)
     May be the first presentation of type 2 diabetes
     Can be a mixed picture with DKA

    Aetiology (precipitants of HHS)


     Infection
    o Major precipitating factor (e.g. pneumonia, urinary tract infections, sepsis)
     Acute illness
    o E.g. CVA (stroke), MI, pancreatitis, Trauma (where counter-regulatory hormones are
    produced – catecholamines, glucagon, cortisol, growth hormone + compromised water
    intake)
     Post-operative (post-CABG or neurosurgery)
     Endocrine
    o Hyperthyroidism, acromegaly, ectopic ACTH, hypercortisolism
     Medications
    o Corticosteroids, thiazide diuretics, beta-blockers, didanosine
    o Discontinued, omitted, or inadequate antihyperglycaemic therapy
     Elderly
    o Bed-ridden causes an altered thirst response that reduces water intake  leads to severe
    dehydration  HHS

    Pathophysiology
     High insulin suppresses lipolysis and ketogenesis but does not regulate blood gluoce production
    and utilisation
     Hyperosmolality inhibits lipolysis, insulin secretion and glucose uptake
     Hypernatraemia + hyperglycaemia + inadequate water intake  hypovolaemic state
     Adrenaline  insulin resistance, decreased insulin production/secretion, increased lipolysis

    Risk factors
     Non-modifibale
    o Age >65 (70 onwards – high mortality risk)
    o Endocrine: Cushing’s syndrome, hyperthyroidism, acromegaly
     Modifiable
    o Poorly controlled diabetes (inadequate insulin/oral antiglycaemic therapy)
    o Acute illness in diabetic patient
    o Infections
    o Post-operative risk
    o Precipitating medications (corticosteroids, thiazides, beta-blockers, didanosine)

    Signs and symptoms


     Diabetes/hyperglycaemia: Polyuria + polydipsia + weight loss + weakness
     Dehydration – poor skin turgor, dry mucous membranes, altered mental status, tachycardia,
    hypotension, shock
     Seizures
     Abdominal pain (more common in DKA than HHS)
     Focal neurological signs (similar to stroke, cresolves rapidly once high BSL is corrected)

    Investigations
     Symptomatic hyperglycaemia (polyuria, polydipsia, abdominal pain, acidotic breath, volume
    depletion, altered mental state) should prompt immediate investigation
    o Plasma glucose
    o Urine ketones
     Bedside
    o Urine ketones – negative/low
    o Urinalysis – positive for gluclose, negative for ketones
    o ECG – hyperkalaemia/hypokalaemia
    o Look for cause – urine/sputum culture (infection)
     Bloods
    o ABG - acidosis
    o FBE – leucocytosis present in hyperglycaemic crisis
    o Blood ketones – negative/low
    o Serum urea and creatinine (UECr) – elevated (volume depletion)
    o Serum sodium – varied
    o Serum potassium – high
    o Serum CMP – low
    o Serum osmolality - >320mmol/kg
    o Look for cause – troponins (MI), blood culture (infection)
     Imaging
    o Look for cause – CXR (pneumonia)

    Prevention
     Primary prevention
    o Contact diabetes care team/GP quickly when symptomatic or high blood sugars on
    glucometer
    o Educate on proper insulin and medication use + carbohydrate diet when nauseated
    o Educate on frequent blood sugar monitoring
    o Eliminate drugs that can precipitate hyperglycaemia

    Acute management
     Fluid replacement therapy – to reduce DIC
     IV insulin – slow infusion with short-acting insulin
    o When serum potassium concentration > 3.5mmol/L
     Potassium replacement
     Phosphate replacement
     SPIDER
    o S: Saline 10-20ml/kg bolus
    o P: Potassium
     High: Give insulin
     Low: Give potassium first, then give insulin
    o I: Insulin
     Actaprapid short acting, continue until normal pH in and normal ketone, usually 12
    hours
    o D: Dextrose
    o E: Embolism (heparin due to VTE risk)
    o E: Eat nothing (NBM)
    o R: Reason  treat cause

    Prognosis
     Mortality rates
    o 5-20%  about 10x higher than DKA
    o Significant mortality risk in people aged >70

    Complications
     Life-threatening: VTE, confusion, DIC, MI, PE, cerebral oedema, coma, stroke
     Treatment-related: Hypoglycaemia, hypokalaemia

    DKA HHS

    Clinical Abdominal pain Confusion/coma Lethargy


    features Nausea, vomiting Weakness, polyuria, polydipsia
    Kussmaul respirations
    Fruity smelling breath
    Coma
    Blood ↑ >13.9 ↑↑ >30.0-33.3
    glucose

    Ketones Ketouria +++ Ketouria +/-


    Blood ketones +++ Blood ketones +/-
    Acid-base pH <7.3 pH normal
    Metabolic acidosis due to No acid-base imbalance
    ketosis
    Serum Variable >320
    osmolality

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