[where not otherwise specified all pictures refer to light microscopy images (1000x magnification) of peripheral blood slides after Wright's staining]

Table of contents : 

hematopoietic organs : spleen osteomyelitis lymph nodes  thymus blood  coagulopathies quantitative alterations in all kinds of blood cells pancytopenias myelodysplastic syndromes (MDS) polycytosis absolute myelodysplastic/myeloproliferative diseases (MDS/MPD) myeloproliferative disorders (MPD) relative alterations in platelets

alterations in RBCs hemorrhages polycythemia alterations in WBCs qualitative alterations quantitative alterations neoplasms infections gas disorders hyperviscosity syndrome hyperosmolality hypoosmolality hypervolemia hypovolemia bibliography web resources associations journals

• alterations in all kinds of blood cells (i.e. impairment of HSC) (cytohaematology)
• quantitative alterations
• pancytopenias : anemia + leukopenia (granulocytopenia (neutropenia + eosinopenia + basophilopenia) + lymphopenia) + thrombocytopenia

Aetiology :
• hypersplenism
• bone marrow failure / medullary aplasia : failure of the hematopoietic function of the bone marrow
• bone marrow suppression / myelophthisis / myelosuppression : suppression of bone marrow activity, resulting in reduction in the number of platelets, red cells, and white cells, such as in aplastic anemia
• radiotherapy
• external beam radiotherapy (EBRT)
• palliative radionuclide therapy of painful bone metastases (RTBM)
• Fanconi's anemia or syndrome
• chronic hypothermia
• osteotabes : a disease, chiefly of infants, in which the cells of the bone marrow are destroyed and the marrow disappears
• during of after viral infection from
• HAV
• HBV
• HCV
• HHV-4 / EBV
• HHV-5 / CMV
• dengue virus
• HIV-1
• parvovirus B₁₉
Pathogenesis :
• virus-induced suppression of HSCs due to direct infection and lysis of the progenitor cells themselves, such as by B₁₉ virus, HHV-5 / CMV, and dengue virus
• altered ability of bone marrow stromal cells to support progenitor cell development due to aberrant stromal cell cytokine expression
• immunosuppressive immune cell cytokines that are released from virally activated cells. For example, TNF-a, TNF-b / LT-a, and IFN-g, induced during virus infection, can influence the development of bone marrow progenitor erythroid and myeloid-lineage cells in vitro.
• myelodysplastic syndromes (MDS) / preukemia
• GR agonists
• polycytosis

Aetiology :
• Cushing's syndrome
• myelodysplastic/myeloproliferative diseases (MDS/MPD)
• myeloproliferative disorders (MPD)
The WHO classification is similar to the FAB and PVSG schemes in that it relies on morphologic, cytochemical, and immunophenotypic features of the neoplastic cells to establish their lineage and degree of maturation. As was true for antecedent classifications, the WHO recognizes the practical importance of the "blast count" in categorizing myeloid diseases and in predicting prognosis. Therefore, the WHO attempts to clearly define "blasts" and to clarify specific issues regarding their accurate and reproducible enumeration. Some of the criteria for blast morphology differ from those in previous classifications. The blast percentage and assessment of degree of maturation and dysplastic abnormalities in the neoplastic cells should be determined, if possible, from a 200-cell leukocyte differential performed on a peripheral blood smear and a 500-cell differential performed on marrow aspirate smears stained with Wright Giemsa or May-Grünwald Giemsa. The blast percentage should be correlated with an estimate of the blast count from the marrow biopsy section. In addition to myeloblasts, the monoblasts and promonocytes in acute monoblastic/monocytic and acute and chronic myelomonocytic leukemia and the megakaryoblasts in acute megakaryoblastic leukemia are considered as "blast equivalents" when the requisite percentage of blasts is calculated for the diagnosis of AML. In acute promyelocytic leukemia (APL), the blast equivalent is the abnormal promyelocyte. This latter cell is usually characterized by a reniform or bilobed nucleus, but its cytoplasm may vary from heavily granulated with bundles of Auer rods to virtually agranular. A recent, detailed morphologic analysis of the abnormal promyelocytes in APL has led to a better appreciation of the cytologic variability of the leukemic cells in this disorder^ref. Erythroid precursors (erythroblasts) are not included in the blast count except in the rare instance of "pure" erythroleukemia. Dysplastic micromegakaryocytes are also excluded from the blast percentage. Although assessment of the number of cells that express the antigen CD34 provides valuable data for diagnostic and prognostic purposes, the percentage of CD34⁺ cells should not be considered a substitute for a blast count from the smears or an estimate from the bone marrow biopsy. Although CD34⁺ hematopoietic cells generally are blasts, not all blasts express CD34^ref. The percentage of blasts proposed by the WHO to categorize a specific case is the percent blasts as a component of all nucleated marrow cells, with the exception of acute erythroleukemia. If a myeloid neoplasm is found concomitantly with another hematologic neoplasmfor example, therapy-related AML and plasma cell myelomathe cells of the nonmyeloid neoplasm should be excluded when blasts are enumerated. Cytochemical studies (myeloperoxidase, nonspecific esterase) and/or immunophenotyping studies (detection of myeloid-related antigens, such as CD117, CD13, CD33) must provide evidence that the neoplastic cells belong to one or more of the myeloid lineages^{ref1, ref2} unless this is obvious from specific morphologic findings, such as Auer rods. (Note: The term "myeloid" refers, in this paper, to bone marrow-derived cells, including granulocytes, monocytes, erythroid, and megakaryocytic lineages.) The WHO classification for AML, MDS, and MPD includes specific genetic subcategories; thus, determination of genetic features of the neoplastic cells must be performed if possible. Many recurring genetic abnormalities in the myeloid neoplasms can be identified by reverse transcriptase-polymerase chain reaction (RT-PCR) or fluorescent in situ hybridization (FISH), but cytogenetic studies should be performed initially and at regular intervals throughout the course of the disease for establishing a complete genetic profile and for detecting genetic evolution. Although it has been suggested that the lack of immediate availability of genetic information is an obstacle to the utilization of the WHO classification^ref, currently available technology should allow assimilation of genetic data in a time frame that will allow appropriate categorization and therapy. It is anticipated that future advances in technology will result in more rapid availability of genetic information.
• alterations in platelets
• alterations in RBCs
• alterations in WBCs
• qualitative alterations
• quantitative alterations
• neoplasms
Laboratory examinations : detection of minimal residual disease (MRD) in acute leukemia patients :
• flow cytometric immunophenotyping
• PCR analysis of antigen receptor genes
• RT-PCR analysis of well-defined chromosomal aberrations with fusion gene transcripts :
• t(1;19) with E2A / TCF3-PBX1
• t(4;11) with MLL-AF4
• t(8;21) with AML1-ETO
• t(9;22) with BCR-c-Abl p190 and BCR-ABL p210
• t(12;21) with TEL / ETV6-AML1
• t(15;17) with PML-RARa
• inv (16) with CBFB-MYH11
• microdeletion 1p32 with SCL interrupting locus (SIL)-TAL1/SCL
PCR primers were designed according to predefined criteria for single PCR (external primers A <--> B) and nested PCR (internal primers C <--> D) as well as for 'shifted' PCR with a primer upstream (E5' primer) or downstream (E3' primer) of the external A <--> B primers. The 'shifted' E primers were designed for performing an independent PCR together with one of the internal primers for confirmation (or exclusion) of positive results. Standardized primer sets with a minimal target sensitivity of 10^-2 for virtually all single PCR analyses, whereas the nested PCR analyses generally reached the minimal target sensitivity of 10^-4. The standardized RT-PCR protocol and primer sets can now be used for molecular classification of acute leukemia at diagnosis and for MRD detection during follow-up to evaluate treatment effectiveness^ref.
Laboratory examinations :
• endothelioid cells (large protoplasmic cells frequently seen in disease of the blood-making organs and believed by some to be derived from the endothelial lining of the blood vessels and lymph vessels)
• abnormal chromatin clumping (ACC) is a sign of severe dysplasia described in the abnormal chromatin clumping syndrome (ACCS), a distinct entity that has both proliferative and trilineal or bilineal dysplastic features^{ref1, ref2}, but it is also present in myelodysplastic syndromes (MDS), reactive dyshemopoiesis^ref, chronic myelogenous leukemia both Ph' positive^ref and negative, and acute myeloid leukemias. Furthermore it has been described in the erythroid and megakaryocyte series, in eosinophils and basophils^ref, in neutrophils as far as the myelocyte stage^ref, in lymphocytes^ref, and in blast cells^ref.
• Infections
• viremia : transient or persistent presence of viruses in blood
• bacteraemias : transient or persistent presence of bacteria in blood
• nosocomial bacteraemias
• Staphylococcus epidermidis (32%)
• Staphylococcus aureus (18.7%)
• Enterococcus (9.8%)
• Escherichia coli (6.9%)
• Klebsiella pneumoniae (5.2%)
• others (21.6%)
• fungemia / mycethemia : transient or persistent presence of fungi in blood
• Paecilomyces lilacinus
• Candida albicans (5.8%)
• Candida dubliniensis
• algaemia : transient or persistent presence of algae in blood
• Prototheca wickerhamii
• parasitemia : transient or persistent presence of protozoa or helminths in blood
Laboratory examination : hemoculture
• Gas disorders
• cyanosis : a bluish discoloration, especially of the skin and mucous membranes due to excessive concentration of deoxyhemoglobin (reduced hemoglobin) in the blood. P_{O2, artery} < 50 mmHg. Cyanosis becomes evident when reduced hemoglobin levels are > 5 g/dl of capillary blood (Lundsgaard C, Van Slyke D. Cyanosis. Medicine (Baltimore) 1923;2:1-76), a value roughly equivalent to 3 g of deoxyhemoglobin/dl of arterial blood^ref. The latter value has been verified by other investigators and has high interrater reliability^ref.
• peripheral cyanosis

Aetiology :
• decreased cardiac output (CO)
• cold exposure
• hemometakinesia
• arterial stenosis
• venous stenosis
• central cyanosis due to failure in pulmonary circulation

Aetiology :
• reduced P_{O2, artery}
• decreased P_{O2, atmosphere} (high altitutides)
• poor oxygenation of the blood in the lungs (pulmonary cyanosis)
• alveolar hypoventilation
• alterated V/Q rate (perfusion of hypoventilated alveola)
• altered O₂ diffusion
• shunt cyanosis : central cyanosis caused by mixing of unoxygenated blood with the arterial blood in the heart or great vessels.
• cyanotic congenital cardiopathies with right=>left shunt (cardiac cyanosis)
• tardive cyanosis : cyanosis in congenital heart disease that appears only after cardiac failure has developed.
• pulmonary arterovenous fistulae
• multiple small intrapulmonary shunts
• hemoglobin with low affinity for O₂ :
• hemoglobin Kansas
• false cyanosis : cyanosis due to the presence of a pigment such as methemoglobin and not to deficient oxygenation of the blood.
• methemoglobinemia : the presence of excessive methemoglobin in the blood

Aetiology :
• congenital or hereditary methemoglobinemia (hereditary methemoglobinemic cyanosis) : any of several rare types caused by inherited conditions
• methemoglobin reductase deficiency
• cytochrome B₅ reductase deficiency is an autosomal recessive condition that may be either confined to the erythrocytes and relatively symptom-free or generalized to the leukocytes and sometimes the brain, muscle, and fibroblasts, in which case the individual may be mentally retarded
• abnormalities of hemoglobin M are autosomal dominant conditions that cause cyanosis in infancy but usually few other symptoms.
• acquired or toxic methemoglobinemia : that caused by exposure to a toxic chemical or drug :
• nitrate and nitrite compounds
• enterogenous cyanosis / Stokvis-Talma syndrome / van den Bergh's disease / autotoxic cyanosis : a syndrome due to absorption of nitrites and sulfides from the intestine, principally marked by methemoglobinemia and/or sulfhemoglobinemia associated with cyanosis. It is accompanied by severe enteritis, abdominal pain, constipation or diarrhea, headache, dyspnea, dizziness, syncope, anemia, and, occasionally, digital clubbing and indicanuria
• centrimide (cetyltrimethylammonium bromide) 0.1% used to treat parasitic splenic cysts
• sulfonamides
• aniline dyes
Low levels of methemoglobin occur in healthy individuals, with typical values ranging from 0.5-2.0%.
Symptoms & signs : while methemoglobinemia can be clinically diagnosed at levels of 1%, methemoglobin levels up to 10% are generally not considered adverse. At levels > 10%, methemoglobinemia causes cyanosis and headache, dizziness, fatigue, ataxia, dyspnea, tachycardia, nausea and vomiting, and drowsiness, which can progress to stupor, coma, and occasionally death by asphyxia at higher concentrations
Therapy : intravenous methylene blue
• sulfhemoglobinemia : the presence of sulfmethemoglobin / sulfhemoglobin (hemoglobin with a sulfur atom on one of its porphyrin rings, so that it is ineffective for transporting oxygen and has a green color) in the blood

Aetiology : excessive exposure to sulfur-containing drugs or other chemicals
Symptoms & signs : cyanosis
• carboxyhemoglobinemia (false cyanosis) : the presence of carboxyhemoglobin (HbCO) (hemoglobin in which the sites usually bound to oxygen are bound to carbon monoxide, which has an affinity for hemoglobin over 200 times that of oxygen) in the blood

Aetiology : tobacco smoking
• differential cyanosis : only in lower limbs, due to persistence of Botallo's duct.
Symptoms & signs : flapping tremor, papilledema, hypertrophic osteoarthropathy (HOA) / acropachy / Marie's disease.
Laboratory examinations : arterial blood gases (ABG)
• hyperviscosity syndrome : any of various syndromes associated with increased viscosity of the blood

Aetiology :
• leukostasis : increased blood viscosity and hypercoagulability, seen in leukemia that is accompanied by hyperleukocytosis
• serum hyperviscosity

Symptoms & signs : spontaneous bleeding with neurologic and ocular disorders
• polycythemia

Symptoms & signs : retarded blood flow, organ congestion, reduced capillary perfusion (weakness, fatigue, bleeding disorders, and visual disturbances), and increased cardiac effort
• conditions in which the deformability of erythrocytes is impaired :
• sickle cell anemia
• plasma hyperosmolality
• hemoconcentration : decrease of the fluid content of the blood, with resulting increase in its concentration

Aetiology :
• exemia : loss of fluid from the blood vessels
• polycythemia
• hyperproteinemia

Aetiology :
• hyperalbuminemia
• relative reduction in serum water (e.g., dehydration)
• hyper-a₁-globulinemia

Aetiology :
• malignancy and acute inflammation
• pregnancy
• hyper-a₂-globulinemia

Aetiology :
• malignancy and acute inflammation
• adrenal insufficiency
• adrenocorticosteroid therapy
• advanced diabetes mellitus
• nephrotic syndrome
• hyper-b-globulinemia

Aetiology :
• biliary cirrhosis
• carcinoma (sometimes)
• Cushing's disease
• diabetes mellitus (some cases)
• hypothyroidism
• iron deficiency anemia
• malignant hypertension
• nephrosis
• polyarteritis nodosa
• obstructive jaundice
• third-trimester pregnancy
• hyperferritinemia (> 2000 ng/ml)  :

Aetiology :
• hematological diseases (45.9%)
• liver diseases (23%)
• chronic renal failure (17.78%)
• neoplastic diseases (10.4%)
• systemic inflammatory diseases (7.4%) : highest values (> 10,000 ng/mL) in adult onset Still's disease (AOSD)
• chronic transfusions (7.4%)
• non-HIV systemic infections (5.9%)
• hyper-g-globulinemia

Aetiology :
• polyclonal gammopathies
• infections
• viral infections, especially hepatitis, human immunodeficiency virus infection, mononucleosis, and varicella
• focal or systemic bacterial infections, including endocarditis, osteomyelitis, and bacteremia
• tuberculosis
• connective tissue disorders
• systemic lupus erythematosus
• mixed connective tissue
• temporal arteritis
• rheumatoid arthritis
• sarcoid
• liver diseases
• cirrhosis
• ethanol abuse
• autoimmune hepatitis
• viral-induced hepatitis
• primary biliary cirrhosis
• primary sclerosing cholangitis
• malignancies
• solid tumors
• ovarian tumors
• lung cancer
• hepatocellular cancer
• renal tumors
• gastric tumors
• hematologic cancers (see below)
• hematologic and lymphoproliferative disorders
• lymphoma
• Hodgkin's disease
• leukemia
• chronic lymphocytic leukemia
• thalassemia
• sickle cell anemia
• other inflammatory conditions
• gastrointestinal conditions, including ulcerative colitis and Crohn's disease
• pulmonary disorders, including bronchiectasis, cystic fibrosis, chronic bronchitis, and pneumonitis
• endocrine diseases, including Graves' disease and Hashimoto's thyroiditis
• monoclonal gammopathies :
• multiple myeloma (M protein appears as a narrow spike in the g, b, or a₂ regions. M-protein level is usually > 3 g/dL. Skeletal lesions (e.g., lytic lesions, diffuse osteopenia, vertebral compression fractures) are present in 80% of patients. Diagnosis requires 10 to 15% plasma cell involvement on bone marrow biopsy. Anemia, pancytopenia, hypercalcemia, and renal disease may be present)
• monoclonal gammopathy of undetermined significance (M-protein level is < 3 g/dL. There is < 10% plasma cell involvement on bone marrow biopsy. Affected patients have no M protein in their urine, no lytic bone lesions, no anemia, no hypercalcemia, and no renal disease.
• smoldering multiple myeloma : M-protein level is > 3 g/dL. There is > 10% plasma cell involvement on bone marrow biopsy. Affected patients have no lytic bone lesions, no anemia, no hypercalcemia, and no renal disease
• plasma cell leukemia : peripheral blood contains > 20% plasma cells. M-protein levels are low. Affected patients have few bone lesions and few hematologic disturbances. This monoclonal gammopathy occurs in younger patients
• solitary plasmacytoma : affected patients have only one tumor, with no other bone lesions and no urine or serum abnormalities
• Waldenström's macroglobulinemia : IgM M protein is present. Affected patients have hyperviscosity and hypercellular bone marrow with extensive infiltration by lymphoplasma cells
• heavy chain disease : the M protein has an incomplete heavy chain and no light chain
• when osmolar gap = (measured plasma osmolality) - (predicted osmotic activity = 2 Na⁺ + Glc + BUN (mmol/L) = 2 Na⁺ (mmol/L) + Glc (mg/dL) / 18 + BUN (mg/dL) / 2.8) > 15-20 mmol/Kg H₂O
• pseudohyponatremia
• accumulation of osmolytes other than Na⁺, Glc, or urea.
• mannitol
• contrast enhancement media
• isopropylic alcohol
• PEG
• ethanol
• methanol
• acetone
• non-ketotic hyperosmolar hyperglycemia (NKHH) in patients with type 2 DM / NIDDM

Epidemiology : elderlies
Aetiology :
• onset of type 2 diabetes mellitus
• inappropriate therapy of type 2 diabetes mellitus (overtreatment with hyperosmolar solutions)
• infections
• acute myocardial infarction (AMI)
• stroke
• thromboembolism
• drugs
• excessive food intake
• traumas
Pathogenesis : less severe hypoinsulinemia with less increased concentration of contrainsular hormones => increased liver glycogenolysis and gluconeogenesis and impaired glucose uptake in skeletal muscle => hyperglycemia => osmotic polyuria => dehydratation (worsened by inefficient water intake) => hemoconcentration => ADH and aldosterone incretion => sodium retention => hypernatremia
=> hyperosmolarity of extracellular fluid => dehydration of intracellular fluid
Symptoms & signs : severe dehydratation => alteration in sensoria or mental obtundation : stupor/coma => hyperosmolar nonketotic coma
Laboratory examinations^ref :
• glycemia > 600 (700-2,200) mg/dL (increased)
• kalemia = 3-5 mEq/L (normal); potassium deficit = 4-6 mEq/kg
• natremia = 130-155 mEq/L (normal); sodium deficit = 100-200 mEq/kg
• pH > 7.30 (7.25-7.4) (normal)
• bicarbonatemia > 15 mEq/l (normal)
• ketonemia = small (0.5-2 mM/L = normal)
• ketonuria = small
• uremia = 30-80 mg/dL (normal or increased)
• plasma osmolality = 2[measured Na (mEq/l)] + glucose (mg/dl)/18 > 320 (340-450) mOsm/kg (increased)
• water deficit = 9 (6-12) L = 100-200 ml/kg
• chloride deficit = 5-15 mEq/l
• phosphate deficit = 3-7 mmol/kg
• magnesium deficit = 1-2 mEq/kg
• calcium deficit = 1-2 mEq/kg
• anion gap =  (Na⁺) - (Cl^- + HCO₃^-) (mEq/l) = variable
Therapy (chronological order) : complete initial evaluation. Start i.v. fluids: 1.0 L of 0.9% NaCl per hour initially =>
• adults (> 20 years)
• potassium :
• if initial kalemia < 3.3 mEq/l, hold insulin and give 40 mEq K+ (2/3 as KCl and 1/3 KPO₄) until K⁺ > 3.3. mEq/l
• if initial serum K+ > 3.3 but < 5.0 mEq/l, give 20-30 mEq K+ in each liter of IV fluid (2/3 as KCl and 1/3 KPO₄) tp keep serum K⁺ at 4-5 mEq/l
• if initial serum K+ > 5.0 mEq/l, do not give K+ but check potassium every 2 h
• regular insulin 0.15 U/kg as IV bolus => 0.1 U/kg/hr IV insulin infusion => check serum glucose hourly. If serum glucose does not fall by at least 50 mg/dl in the first hour, then double insulin dose hourly until glucose falls at a steady hourly rate of 50-70 mg/dl => check electrolytes, BUN, creatinine and glucose every 2-4 h until stable. After resolution of HHS, if the patient is NPO, continue IV insulin and supplement with SC  regular insulin as needed. When the patient can eat, initiate SC insulin or previous treatment regimen and assess metabolic control. Continue to look for precipitating cause(s) => change to 5% dextrose with 0.45% NaCl and decrease insulin to 0.05-0.1 units/kg/hr to maintain serum glucose between 250-300 mg/dl until plasma osmolality is < 315 mOsm/kg and patient is mentally alert
• IV fluids => determine hydration status =>
• hypovolemic shock => administer 0.9% NaCl (1.0 L/h) and/or plasma expanders
• mild hypotension => evaluate corrected natremia =>
• hypernatremia or normonatremia => 0.45% NaCl (4-14 ml/kg/hr) depending on state of hydration => when serum glucose reaches 300 mg/dl => change to 5% dextrose with 0.45% NaCl and decrease insulin to 0.05-0.1 units/kg/hr to maintain serum glucose between 250-300 mg/dl until plasma osmolality is < 315 mOsm/kg and patient is mentally alert
• hyponatremia => 0.9% NaCl (4-14 ml/kg/hr) depending on state of hydration => when serum glucose reaches 300 mg/dl => change to 5% dextrose with 0.45% NaCl and decrease insulin to 0.05-0.1 units/kg/hr to maintain serum glucose between 250-300 mg/dl until plasma osmolality is < 315 mOsm/kg and patient is mentally alert
• pediatric patients (< 20 years) :
• IV fluids => determine hydration status =>
• hypovolemic shock => administer 0.9% NaCl (20 ml/kg/h) and/or plasma expanders until shock resolved
• mild hypotension => administer 0.9% NaCl (10 ml/kg/h) for initial hour =>
• replace fluid deficit evenly over 48 h with 0.45-0.9% NaCl => when serum glucose reaches 250 mg/dl => change to 5% dextrose with 0.45-0.75% NaCl, at a rate to complete rehydration in 48 h and to maintain glucose between 150-250 mg/dl (10% dextrose with electrolytes may be required) => check glucose and electrolytes every 2-4 h until stable. Look for precipitating causes. After resolution of DKA, initiate SC insulin (0.5-1.0 U/kg/d given as 2/3 in the a.m. [1/3 short-acting, 2/3 intermediate-acting], 1/3 in p.m. [1/2 short-acting, 1/2 intermediate-acting]) or as 0.1-0.25 U/kg regular every 6-8 hours during the first 24 hours for new patients to determine insulin requirements
• insulin =>
• IV route => IV insulin infusion : regular insulin 0.1 U/kg/h => continue until acidosis clears (pH > 7.3, HCO₃ > 15) => decrease to 0.05 U/kg/h until SC insulin replacement intiated
• IM (if no IV access) : regular insulin 0.1 U/Kg IV bolus followed by 0.1 U/kg/hr SC or IM
• potassium
• K⁺ < 2.5 mEq/l => administer 1 mEq/kg of KCL in IV over 1 h. Withhold insulin until K⁺> 2.5
• K⁺ 2.5-3.5 mEq/l => administer K⁺ 40-60 mEq/l in IV solution until K+ > 3.5. Monitor K⁺ hourly => check results of hourly K+ monitoring =>
• K⁺ < 2.5 mEq/l => see above
• K⁺ = 2.5-3.5 mEq/l => continue as above
• K⁺ > 3.5 mEq/l => see below
• K⁺ 3.5-5.5 mEq/l => administer K⁺ 30-50 mEq/l in IV solution to maintain serum K⁺ at 3.5-5.5 mEq/l
• assess need for bicarbonate =>
• pH < 7.0 => repeat pH after initial hydration bolus =>
• pH < 7.0 => over 1 h, administer NaHCO₃ (2 mEq/kg) added to NaCl to produce a solution that does not exceed 155 mEq/l of Na over 1 hr
• pH > 7.0 => see below
• pH > 7.0 => no HCO₃ indicated
• plasma hypoosmolality

Aetiology :
• hypotonic syndromes : a group of syndromes involving inadequate water excretion in comparison to the amount ingested, so that body fluids become hypotonic and hyponatremic; some are due to excessive water intake as in water intoxication, while others are caused by derangements of the excretory process such as the vasopressin excess in the syndrome of inappropriate diuretic hormone or complications of the nephrotic syndrome, congestive heart failure, or kidney failure.
• hypoproteinemia
• hypoalbuminemia

Aetiology :
• hormone therapy
• pregnancy
• burns
• chronic cachectic or wasting diseases
• chronic infections
• hemorrhage, burns, or protein-losing enteropathy
• liver failure resulting from decreased synthesis of albumin
• malnutrition
• proteinuria
• hypo-a₁-globulinemia

Aetiology :
• a₁-antitrypsin deficiency
• liver failure
• hypo-a₂-globulinemia

Aetiology :
• malnutrition
• megaloblastic anemia
• protein-losing enteropathy
• severe liver failure
• Wilson's disease 
• hypo-b-globulinemia

Aetiology :
• protein malnutrition
• hypo-g-globulinemia

Aetiology :
• agammaglobulinemia
• hypogammaglobulinemia
Laboratory examinations :
• serum protein electrophoresis : indications
• suspected multiple myeloma, Waldenström's macroglobulinemia, primary amyloidosis, or related disorder
• unexplained peripheral neuropathy (not attributed to longstanding diabetes mellitus, toxin exposure, chemotherapy, etc.)
• new-onset anemia associated with renal failure or insufficiency and bone pain
• back pain in which multiple myeloma is suspected
• hypercalcemia attributed to possible malignancy (e.g., associated weight loss, fatigue, bone pain, abnormal bleeding)
• rouleaux formations noted on peripheral blood smear
• renal insufficiency with associated serum protein elevation
• unexplained pathologic fracture or lytic lesion identified on radiograph
• Bence Jones proteinuria
• immunofixation also should be performed because this technique may be more sensitive in identifying a small monoclonal (M) protein.5
• hypervolemia

Aetiology :
• endovenous therapy
• acute renal failure (ARF)
• primary hyperaldosteronism
• hypovolemia : decreased plasma volume (associated with hyponatremia, eunatremia, or hypernatremia)

Aetiology :
• decreased extracellular compartment volume
• extrarenal sodium loss
• gastrointestinal sodium loss : vomiting, nasogastric probe, diarrhea
• sweat sodium loss : fever defervescence, prolonged heat exposure, physical exercise
• respiratory airways sodium loss : hyperventilation in febrile patients with assisted ventilation
• hemorrhages
• renal sodium and water loss due to polyuria
• diuretics
• osmotic diuresis
• transient, due to expansion of extracellular compartment due to oliguria
• polyuria during acute tubular necrosis
• removal of bilateral obstructive uropathy
• hypoaldosteronism
• renal water loss (less severe hypovolemia as 66% of water depletion occurs in intracellular volume)
• diabetes insipidus
• normal or increased volume of extracellular compartment
• decreased cardiac output due to cardiopathies
• redistribution
• exit of fluid from capillaries into interstitium (edema)
• exit of fluid from capillaries into "third space" (a compartment not in equilibrium with ECF nor ICF)
• subcutaneous tissue during severe burn wound
• intestinal lumen during intestinal occlusion
• retroperitoneal space in acute pancreatitis
• peritoneal cavity in peritonitis
• intestinal ischemia
• rhabdomyolysis
• increased venous capacitance : sepsis, varices and pregnancy
Pathogenesis : decreased preload => decreased CO => systemic arterial hypotension => activation of baroreceptors => activation of sympathetic nervous system and RAA system to maintain average arterial pressure and cerebral and coronary perfusions.
Symptoms & signs : astheny, fatigue, muscular cramping, thirst, orthostatic pressure instability, organ ischemia (=> oliguria or prerenal acute renal failure, cyanosis, chest or abdominal pain, confusion, obnubilation of sensations), mouth and skin dryness, decreased jugular pressure, orthostatic hypotension and tachycardia => hypovolemic shock
Laboratory examination : urine osmolality > 450 mosm/L and urine density > 1.015 (except in hypovolemia due to diabetes insipidus)
Therapy : p.o. or i.v. isotonic (NaCl 0.9% or 154 mmol/L Na⁺) or hypertonic (to correct hyponatremia : NaCl 3% or 513 mmol/L Na⁺) or hypotonic (to correct hypernatremia : NaCl 0.45% or 77 mmol/L Na⁺) solution
• Animal models and cell lines :
• BCL1 tumor in the spleen
• J558 tumor in the subcutaneous space

Copyright © 2001-2005 Daniele Focosi. All rights reserved  |  Terms of use  | Legal notices
About this site  |  Site map  |  Acknowledgements | Open forum  |  Tell a friend about this site  |  Current link partners
 Abbreviations and acronyms  |  Medical terminology  |  Add a link  |  Translate this site into your favourite language  |  Softwares

---