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253.e2  Diabetes, Hyperosmolar Hyperglycemic State




            Diabetes, Hyperosmolar Hyperglycemic State                                             Client Education
                                                                                                         Sheet
  VetBooks.ir

            BASIC INFORMATION
                                              •  Altered neurologic status (e.g., convulsions,
                                                                                   hypophosphatemia, and hypernatremia) can
                                                ataxia, muscle twitching, nystagmus, lethargy,   abnormalities (hyperkalemia or hypokalemia,
           Definition                           coma)                              be seen.
           •  A hyperosmolar hyperglycemic state (HSS) is   •  Decreased body condition score common  •  Urinalysis:  ± ketones (ketones present in
            a life-threatening but uncommon metabolic   •  Bradycardia if hyperkalemia is present  ≈30%); may see pyuria, bacteriuria (cystitis)
            state characterized by marked hyperglycemia   •  ± Fever             •  Ketones can be measured in serum, plasma,
            and  hyperosmolarity  and  resulting  from                             or urine.
            uncontrolled diabetes mellitus (DM).  Etiology and Pathophysiology     ○   Although two ketone bodies formed
           •  Although most often identified in animals   •  An absolute or relative reduction in circula-  in DKA (acetone and acetoacetate) are
            lacking ketone production (i.e., hyperosmolar   ting insulin combined with increased coun-  readily detected on a urine dipstick by the
            nonketotic [HNK] diabetes), HHS can also   terregulatory hormones is key to development   nitroprusside reaction, the predominant
            occur concurrently with diabetic ketoacidosis   of HHS and DKA.          ketone body (beta-hydroxybutyrate) is not
            (DKA). In other words, animals with HSS   •  Ketones are not produced if sufficient insulin   detected.
            may or may not have ketosis.        is present to inhibit lipolysis and ketogenesis   •  Urine  culture  and  susceptibility:  rule  out
                                                (as in type II DM) or when hyperosmolarity   secondary urinary tract infection
           Synonyms                             inhibits lipolysis, thereby limiting the amount   •  Additional  diagnostics,  including  thoracic
           Hyperosmolar nonketonuric (HNK or HONK)   of free fatty acids available for ketogenesis.  or abdominal  imaging,  may be necessary
           diabetes mellitus, hyperosmolar nonketotic   •  In people, HNK is more common in type II   based on clinical signs to rule out concurrent
           diabetes                             DM; although insulin is deficient, there is   diseases.
                                                enough to inhibit lipolysis and ketogenesis
           Epidemiology                         but not enough to prevent hyperglycemia.   Advanced or Confirmatory Testing
           SPECIES, AGE, SEX                    Cats are more likely than dogs to have   •  Marked increase in serum osmolality (usually
           •  More common in cats than dogs but occurs   residual insulin secretion despite being   > 340 mOsm/kg; typical reference range is
            in both species.                    diabetic, perhaps explaining why HNK is   285-308 mOsm/kg for cats and dogs)
           •  Usually middle-aged to older pets  more common in cats than dogs.    ○   Can be measured or calculated
                                              •  Hyperosmolarity  may  decrease  lipolysis,   ○   Calculated: Osm = 2(Na + K) + [Glu/18]
           GENETICS, BREED PREDISPOSITION       limiting the amount of free fatty acids   + [BUN/2.8]
           Australian terrier, Samoyeds, Bichon frisé,   available for ketogenesis.
           standard and miniature schnauzers, miniature   •  Depressed mental status in HHS patients    TREATMENT
           and toy poodles, and spitz dogs are at increased   is attributed to hypernatremia and hyperos-
           risk for DM.                         molarity-induced dehydration of the brain   Treatment Overview
                                                parenchyma. Although measured sodium   Rehydration and correction of electrolyte
           RISK FACTORS                         levels are rarely dramatically increased with   disturbances is the initial step in treating HHS
           •  Unregulated DM                    HHS, a corrected sodium level in relation   patients. After this is accomplished, insulin
           •  Concurrent infection or illness in diabetic   to hyperglycemia can be high enough to   therapy is initiated to gradually decrease blood
            patient                             indicate cellular dehydration and neurologic   glucose (BG) concentrations.
                                                disruption (see below).
           ASSOCIATED DISORDERS                                                  Acute General Treatment
           •  DKA                              DIAGNOSIS                         •  Rehydration with isotonic crystalloid fluids
           •  Kidney failure (acute or chronic)                                    is essential. Isotonic saline (0.9% NaCl) is
           •  Cardiac disease, including congestive heart   Diagnostic Overview    typically used because it addresses fluid
            failure                           Diagnosis of HHS is based on documenta-  deficits and replaces glucose with sodium
           •  Neoplasia                       tion of hyperglycemia (typically extreme) and   in the extracellular space, preventing a rapid
           •  Gastrointestinal (GI) disease   hyperosmolarity; if ketones are absent, the term   shift in osmolality. Isotonic saline can also
           •  Pancreatitis                    HNK also applies. HHS can occur in patients   help prevent overly rapid reduction in serum
           •  Respiratory disease             with newly recognized DM or in patients with   sodium (do not lower Na by more than
           •  Acromegaly (cats)               known DM.                            1 mEq/L/h)
                                                                                   ○   Can  begin  with  fluid  bolus  of  20 mL/
           Clinical Presentation              Differential Diagnosis                 kg  (cat)  or  30 mL/kg  (dog)  to  address
           HISTORY/CHIEF COMPLAINT            •  Vomiting, inappetence, lethargy can be due to   shock and hypovolemia. This bolus may
           Animals may (≈50%) or may not have a   a concurrent disease (e.g., DKA, pancreatitis,   be repeated based on clinical response
           history of previously recognized clinical signs   severe infection)       (e.g., capillary refill time, blood pressure,
           of DM (i.e., polyuria/polydipsia, polyphagia,   •  Depressed mental status: intracranial disease   mentation status)
           and weight loss). Historical findings related   (e.g., neoplasia, granulomatous inflamma-  ○   After crisis of vascular volume is addressed,
           specifically to HHS include:         tion, infarct), hypoglycemia, other severe   correct dehydration deficit. Dehydration
           •  Inappetence                       illness                              deficit is calculated as body weight (kg)
           •  Vomiting                                                               × % estimated dehydration (as decimal);
           •  Lethargy (often severe)         Initial Database                       for example, a 10-kg animal that is 8%
           •  Behavioral changes              •  CBC: neutrophilia as part of stress leukogram   dehydrated = 10 × 0.08 = 0.8 L deficit.
           •  Rarely, coma                      related to HHS or indication of a secondary   ○   Correct one-half of deficit within 12 hours
                                                infection.  Moderate  anemia  if  significant   and remainder over the next 24 hours.
           PHYSICAL EXAM FINDINGS               hypophosphatemia is present.       ○   After  restoration  of  vascular  volume,
           •  Severe dehydration (>8%)        •  Serum  chemistry:  hyperglycemia  (often   fluid type may be changed to a more
           •  Depressed or obtunded mentation   >  800 mg/dL),  azotemia,  and  electrolyte   physiologic isotonic fluid (e.g., lactated
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