- Old samples cause RBCs to swell, thus increasing PCV and MCV and decreasing MCHC.
- Lipemia causes a falsely high Hgb reading, and hence a falsely high MCHC.
- Hemolysis causes PCV to decrease while Hgb remains unchanged, again leading to a falsely high MCHC
- Underfilling of the tube causes RBCs to shrink, causing PCV and MCV to decrease and MCHC to increase.
- Autoagglutination causes a falsely low RBC count, and hence a falsely high MCV.
Clinical Hematology
Hip fracture
A
hip fracture is one of the most serious consequences of falls in the elderly,
with a mortality of 10% at one month and 30% at one year.
There
is also significant morbidity associated with hip fractures, with only 50%
returning to their previous level of mobility and 10 to 20% of patients being
discharged to a residential or nursing care placement.
Up
to 20% of patients with hip fractures will develop a postoperative complication,
with chest infections (9%) and heart failure (5%) being the most common.
Developing
heart failure following a hip fracture has a very poor prognosis, with a one-year
mortality of 92% and a 30-day mortality of 65%.
For
chest infections, the one-year mortality is 71% and 43% within 30 days.
The
effect of timing of surgical intervention on mortality remains a controversial
topic. Various studies have demonstrated an improvement in mortality following
early surgical intervention, but other studies did not. However, there is
widespread evidence that early operative intervention does improve outcomes,
including morbidity (especially infections), pressure sores, pain, and length
of stay.
Circle of Willis
The
Circle of Willis is an arterial polygon (heptagon) formed as the internal
carotid and vertebral systems anastomose around the optic chiasm and
infundibulum of the pituitary stalk in the suprasellar cistern. This
communicating pathway allows equalization of blood-flow between the two sides
of the brain, and permits anastomotic circulation, should a part of the
circulation be occluded.
A complete circle of Willis (in which no component is absent or hypoplastic) is only seen in 20-25% of individuals. Posterior circulation anomalies are more common than anterior circulation variants and are seen in nearly 50% of anatomical specimens.
Hemochromatosis
Hemochromatosis is a disorder associated with deposits
of excess iron that causes multiple organ dysfunction. Hemochromatosis has been
called “bronze diabetes” due to the discoloration of the skin and associated
disease of the pancreas. Hereditary hemochromatosis is the most common
autosomal recessive disorder in whites. Secondary hemochromatosis occurs
because of erythropoiesis disorders and treatment of the diseases with blood
transfusions.
A common initial presentation is an asymptomatic
patient with mildly elevated liver enzymes who is subsequently found to have
elevated serum ferritin and transferrin saturation. Ferritin levels greater
than 300 ng per mL for men and 200 ng per mL for women and transferrin
saturations greater than 45% are highly suggestive of hereditary
hemochromatosis.
Phlebotomy is the mainstay of treatment and can help
improve heart function, reduce abnormal skin pigmentation, and lessen the risk
of liver complications. Liver transplantation may be considered in select
patients. Individuals with hereditary hemochromatosis have an increased risk of
hepatocellular carcinoma and colorectal and breast cancers. Genetic testing for
the hereditary hemochromatosis genes should be offered after 18 years of age to
first-degree relatives of patients with the condition.
Brain natriuretic peptide
Brain natriuretic peptide
BNP is initially synthesized as a 134–amino-acid
peptide called pre-pro BNP. The secondary cleaving of a 26–amino-acid signal
peptide results in the formation of pro-BNP or BNP 1-108. This molecule is
cleaved by furin, an endo-protease, into BNP 32 and N-terminal BNP (NT-BNP
1-76).
Major points to remember regarding BNP and NT-proBNP include:
- A major application of both BNP and proBNP testing is the evaluation of patients with congestive heart failure. If heart failure responds to therapy, concentrations of BNP and NT-proBNP should decline, indicating progress of therapy. If a patient does not respond, values may be increased gradually.
- In general, NT-proBNP is more stable (up to seven days at room temperature and up to four months if stored at −20°C) than BNP, which is not stable for a day even if the specimen is stored in a refrigerator. Therefore, BNP analysis must be performed as soon as possible after collecting the specimen.
- The cut-off level of BNP and NT-proBNP depends on age, as values tend to increase with advancing age. In general, heart failure is unlikely if the BNP value is less than 100 pg/mL and heart failure is very likely if the value is over 500 pg/mL. For NT-proBNP, the normal value for a person 50 years or younger is usually 125 ng/mL, but heart failure is unlikely if the NT-proBNP value is<300 pg/mL. However, heart failure is likely if the value is>450 pg/mL (>900 pg/mL in a patient of age 50 and above).
- Patients with end-stage renal disease and dialysis patients usually show higher BNP and NT-proBNP in serum than normal individuals.
Malnutrition
Malnutrition is an imbalance between the nutrients your body needs to function and the nutrients it gets. It is an independent risk factor that negatively influences patients’ clinical outcomes, quality of life, body function, and autonomy. Early identification of patients at risk of malnutrition or who are malnourished is crucial in order to start a timely and adequate nutritional support. Nutrition support refers to enteral or parenteral provision of calories, protein, electrolytes, vitamins, minerals, trace elements, and fluids.
Historically, serum proteins such as albumin and prealbumin (i.e. transthyretin) have been widely used by physicians to determine patients’ nutritional status. Other markers that have been studied include retinol-binding protein (RBP), transferrin, total cholesterol and indicators of inflammation such as C-reactive protein (CRP) and total lymphocyte count (TLC).
Aortic valve stenosis
Among
symptomatic patients with medically treated moderate-to-severe aortic stenosis,
mortality from the onset of symptoms is approximately 25% at 1 year and 50% at
2 years. Symptoms of aortic stenosis usually develop gradually after an
asymptomatic latent period of 10-20 years.
Systolic
hypertension can coexist with aortic stenosis. The carotid arterial pulse
typically has a delayed and plateaued peak, decreased amplitude, and gradual
downslope (pulsus parvus et tardus).
Other
symptoms of aortic stenosis include the following:
- Pulsus alternans: Can occur in the presence of left ventricular systolic dysfunction
- Hyperdynamic left ventricle: Unusual; suggests concomitant aortic regurgitation or mitral regurgitation
- Soft or normal S1
- Diminished or absent A2: The presence of a normal or accentuated A2 speaks against the existence of severe aortic stenosis
- Paradoxical splitting of the S2: Resulting from late closure of the aortic valve with delayed A2
- Accentuated P2: In the presence of secondary pulmonary hypertension
- Ejection click: Common in children and young adults with congenital aortic stenosis and mobile valve leaflets
- Prominent S4: Resulting from forceful atrial contraction into a hypertrophied left ventricle
- Systolic
murmur: The classic crescendo-decrescendo systolic murmur of aortic stenosis
begins shortly after the first heart sound; the intensity increases toward mid
systole and then decreases, with the murmur ending just before the second heart
sound.
Lasix (Furosemide)
- Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule.
- Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium.
- Effectiveness persists in impaired renal function.
- Absorption: 60–67% absorbed after oral administration (↓ in acute HF and in renal failure); also absorbed from IM sites; IV administration results in complete availability; 99.6% absorbed after SUBQ administration.
- Protein Binding: 91–99%.
- Metabolism and Excretion: Minimally metabolized by liver, some non-hepatic metabolism, some renal excretion as unchanged drug.
- Half-life: 30–120 min (↑ in renal impairment).
Peritonitis
Peritonitis is defined as an inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. Depending on the underlying pathology, the resultant peritonitis may be infectious or sterile (ie, chemical or mechanical).
Peritoneal infections are classified as primary (ie, from hematogenous dissemination, usually in the setting of an immunocompromised state), secondary (ie, related to a pathologic process in a visceral organ, such as perforation or trauma, including iatrogenic trauma), or tertiary (ie, persistent or recurrent infection after adequate initial therapy). Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) seen mostly in with chronic liver disease. Secondary peritonitis is by far the most common form of peritonitis encountered in clinical practice. Tertiary peritonitis often develops in the absence of the original visceral organ pathology.
Infections
of the peritoneum are further divided into generalized (peritonitis) and
localized (intra-abdominal abscess).
Hypomagnesemia
Hypomagnesemia
is common among hospitalized patients and frequently occurs with other
electrolyte disorders, including hypokalemia and hypocalcemia. Magnesium
depletion usually results from inadequate intake plus impairment of renal
conservation or gastrointestinal absorption.
Drugs
can cause hypomagnesemia. Examples include chronic (> 1 year) use of a
proton pump inhibitor and concomitant use of diuretics. Amphotericin B can
cause hypomagnesemia, hypokalemia, and acute kidney injury. The risk of each of
these is increased with duration of therapy with amphotericin B and concomitant
use of another nephrotoxic agent. Liposomal amphotericin B is less likely to
cause either kidney injury or hypomagnesemia.
Trousseau
sign is the precipitation of carpal spasm by reduction of the blood supply to
the hand with a tourniquet or blood pressure cuff inflated to 20 mm Hg above
systolic blood pressure applied to the forearm for 3 minutes.
Chvostek
sign is an involuntary twitching of the facial muscles elicited by a light
tapping of the facial nerve just anterior to the exterior auditory meatus.
Serum
magnesium concentration < 1.8 mg/dL
Hypomagnesemia
is diagnosed by measurement of serum magnesium concentration.
Severe
hypomagnesemia usually results in concentrations of < 1.25 mg/dL.
Associated
hypocalcemia and hypocalciuria are common.
Hypokalemia
with increased urinary potassium excretion and metabolic alkalosis may be
present.
Treatment
with magnesium salts is indicated when magnesium deficiency is symptomatic or
the magnesium concentration is persistently < 1.25 mg/dL. Patients with
alcohol use disorder are treated empirically. In such patients, deficits
approaching 12 to 24 mg/kg are possible.
Procalcitonin (PCT)
Procalcitonin (PCT) has developed into a promising new biomarker for early detection of (systemic) bacterial infections. PCT is a 116-amino acid residue that was first explained by Le Moullec et al. in 1984; however, its diagnostic significance was not recognized until 1993. In 1993, Assicot et al. demonstrated a positive correlation between high serum levels of PCT and patients with positive findings for bacterial infection and sepsis (eg, positive blood cultures). PCT assays with a specificity of 79%, is utilized to more accurately determine if a bacterial species is the cause of a patient’s systemic inflammatory reaction.
Procalcitonin serum levels have been shown to increase 6 to 12 hours following initial bacterial infections and increase steadily 2 to 4 hours following the onset of sepsis. The half-life of PCT is between 20 to 24 hours; therefore, when a proper host immune response and antibiotic therapy are in place, PCT levels decrease accordingly by 50% over 24 hours.
PCT
serum levels can become elevated among patients during times of noninfectious
conditions, such as with trauma, burns, carcinomas (medullary C-cell, small
cell lung, & bronchial carcinoid), immunomodulator therapy that increase
proinflammatory cytokines, cardiogenic shock, first 2 days of a neonate's life,
during peritoneal dialysis treatment, and in cirrhotic patients (Child-Pugh
Class C). Furthermore, PCT levels have found to be falsely elevated in patients
suffering from various degrees of chronic kidney disease which can, in turn,
alter baseline results making the determination of an underlying bacterial
infection difficult to establish.