Page 1033 - Cote clinical veterinary advisor dogs and cats 4th

510 Hyperviscosity Syndrome

ASSOCIATED DISORDERS abnormalities warrants further evaluation to • Immunoelectrophoresis: further evaluation
• Neurologic signs from sludging of blood identify the underlying condition. Establishing of a monoclonal gammopathy to assess
VetBooks.ir • Retinal lesions for optimal treatment. Serum viscosity can be • Bence Jones proteinuria if hyperglobulinemia
concentrations of specific immunoglobulins
a specific diagnosis (see list above) is essential
• Bleeding disorders from platelet and coagula-
tion factor inhibition
measured by a reference laboratory, but the
is cause of hyperviscosity
• Volume overload and congestive heart failure
on the underlying cause.
urine
• Azotemia from decreased renal perfusion, clinical utility is low because treatment depends ○ Excessive immunoglobulin light chains in
infiltrative renal lesions, or associated ○ May be present with multiple myeloma,
hypercalcemia Differential Diagnosis CLL, Waldenström’s macroglobulinemia,
• Immune suppression and secondary infection • Lethargy, weakness, weight loss, polyuria/ or plasma cell leukemia
• Pathologic fractures from infiltrative bone polydipsia are nonspecific signs, typically ○ Alternatively, urine protein electrophoresis
lesions (myeloma) investigated with a CBC, serum biochemical may be performed.
profile, and urinalysis to identify abnormali- • Coagulation profile: bleeding disorders, espe-
Clinical Presentation ties responsible for hyperviscosity. cially platelet dysfunction (elevated buccal
HISTORY, CHIEF COMPLAINT • Acute visual deficits: retinal detachment, mucosal bleeding time; normal prothrombin
• Various combinations and severity of: retinal hemorrhage, sudden acquired retinal time, activated partial thromboplastin time)
lethargy, weakness, weight loss, polyuria/ degeneration may occur with hyperglobulinemia. Indicated
polydipsia, neurologic deficits, collapse, • Acute neurologic deficit: encephalitis, intra- if bleeding (epistaxis, petechia, hyphema,
blindness, and overt bleeding cranial hemorrhage, hepatic encephalopathy retinal hemorrhage) occurs.
• Blood may be thick and difficult to collect • Difficult phlebotomy: hypovolemia, technical • Bone marrow aspirate ± core biopsy: > 20%
by phlebotomy (especially from peripheral difficulties often abnormal plasma cells in multiple
veins). myeloma or plasma cell leukemia (p. 1068)
Initial Database • Echocardiogram (p. 1094) with microbubble
PHYSICAL EXAM FINDINGS • CBC: markedly elevated hematocrit (i.e., contrast: to identify right ventricular hyper-
Ocular changes (retinal vessel engorgement/ > 60%) suggests erythrocytosis as cause trophy and right-to-left cardiac shunt
tortuosity, retinal hemorrhage or detachment, of hyperviscosity; lymphocytosis may be • Ehrlichia canis titer, Leishmania direct aggluti-
papilledema), neurologic deficits (blindness, apparent with leukemia. nation test; others: as indicated by geographic
altered mentation), epistaxis, mucosal hemor- • Serum biochemistry profile: hyper- exposure and other clinical features
rhage or ecchymoses, or lymphadenopathy. If globulinemia if hyperviscosity caused by
erythrocytosis present, red or cyanotic mucous Waldenström’s macroglobulinemia, multiple TREATMENT
membranes myeloma, FIP, amyloidosis, or ehrlichiosis
and possibly with CLL Treatment Overview
Etiology and Pathophysiology • Urinalysis: no specific findings. Bence Jones Hyperviscosity syndrome is a secondary
Viscosity is a function of the concentration proteins associated with multiple myeloma condition. Patients may present with signs of
and composition of blood components. A are not detected on routine urinalysis. hyperviscosity (e.g., epistaxis, blindness, retinal
marked increase in plasma proteins or blood • Retinal exam: retinal arteries may be enlarged hemorrhage) and/or signs of the underlying
cells raises viscosity, leading to sludging in the or tortuous; signs of uveitis or chorioretinitis condition. Identifying and treating the primary
microcirculation, causing clinical manifesta- may be present in FIP. disease process is the cornerstone of care.
tions. Hyperviscosity may present insidiously Acutely, provide adequate hydration, supply
with vague signs or acutely with neurologic Advanced or Confirmatory Testing tissue oxygenation, and ensure appropriate
and/or ophthalmic deficits. • Serum or whole blood viscosity: measured by urine production. Phlebotomy or apheresis
Hyperviscosity syndrome can be caused by one a reference laboratory to confirm hyperviscos- to reduce circulating blood components con-
of several hematologic conditions: ity syndrome; rarely tested tributing to hyperviscosity syndrome may be
• Multiple myeloma (IgG or IgA) • Blood pressure measurement (p. 1065): used immediately if clinical signs are severe
• Waldenström’s macroglobulinemia (IgM) systemic hypertension may result from before definitive therapy for underlying
• Plasma cell leukemia hyperglobulinemia. condition.
• Lymphoma • Thoracic radiographs: lytic bone lesions
• Chronic lymphocytic leukemia (CLL) can be observed with multiple myeloma or Acute General Treatment
• Amyloidosis rarely with lymphoma. Pulmonary changes • To alleviate clinically significant neurologic
• Infectious disease: feline infectious peritonitis if hypoxemia is the cause of secondary or ophthalmic signs, phlebotomy is used to
(FIP), ehrlichiosis, leishmaniasis erythrocytosis reduce the hematocrit to < 60%.
• Primary erythrocytosis (polycythemia vera) • Abdominal ultrasound ○ Remove up to 10-20 mL/kg whole blood
• Secondary erythrocytosis ○ Diffuse hepatosplenomegaly or lymph- (jugular vein preferred), with replacement
○ Hypoxemia (e.g., right-to-left patent adenopathy may be present with lymphoma, of equivalent volume of isotonic crystal-
ductus arteriosus, elevated altitude, ehrlichiosis, or multiple myeloma (mainly loids (peripheral IV catheter preferred).
chronic pulmonary disease) splenomegaly). ○ If hypovolemia (tachycardia, weak pulses,
○ Neoplasia (renal tumors, rarely sarcomas) ○ Renal neoplasm (source of excess hypotension, obtundation) develops, more
erythropoietin) as source of secondary conservative phlebotomy volumes and
DIAGNOSIS erythrocytosis more aggressive crystalloid replacement
• Serum protein electrophoresis (p. 1375): are indicated during the initial treatments.
Diagnostic Overview monoclonal protein spike with Waldenström’s • When hyperglobulinemia is the cause of
History and physical exam findings should macroglobulinemia, multiple myeloma, or hyperviscosity, withdrawn blood can be
raise suspicion; the clinical triad of neurologic, plasma cell leukemia or rarely with CLL. centrifuged and autologous red blood
ophthalmic, and hemorrhagic findings suggests Polyclonal gammopathy usually with FIP, cells returned after discarding the plasma
possible hyperviscosity. Diagnosis is further sup- amyloidosis, or ehrlichiosis but occasionally component. Alternatively, plasmapheresis
ported by routine CBC and serum biochemistry monoclonal. Urine electrophoresis may reveal or therapeutic plasma exchange can be
profile showing severe leukocytosis, erythro- monoclonal spike for neoplastic disorders performed when patients have severe clinical
cytosis, or hyperglobulinemia. Any of these (less commonly used). signs.

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