Fungus
Sepsis
Total Organ Failure
Illegal Organ Transplant
Left shift or blood shift is an increase in the number of immature cell types among the blood cells in a sample of blood. Many (perhaps most) clinical mentions of left shift refer to the white blood cell lineage, particularly neutrophil-precursor band cells,[1] thus signifying bandemia. Less commonly, left shift may also refer to a similar phenomenon in the red blood cell lineage in severe anemia, when increased reticulocytes and immature erythrocyte-precursor cells appear in the peripheral circulation.[2]
The standard definition of a left shift is an absolute band form count greater than 7700/microL.[3] There are competing explanations for the origin of the phrase "left shift," including the left-most button arrangement of early cell sorting machines[4][5] and a 1920s publication by Josef Arneth, containing a graph in which immature neutrophils, with fewer segments, shifted the median left.[6] In the latter view, the name reflects a curve's preponderance shifting to the left on a graph of hematopoietic cellular differentiations.
It is usually noted on microscopic examination of a blood smear. This systemic effect of inflammation is most often seen in the course of an active infectionand during other severe illnesses such as hypoxia and shock.
It is believed that cytokines (including IL-1 and TNF) accelerate the release of cells from the postmitotic reserve pool in the bone marrow, leading to an increased number of immature cells.[1]
https://en.wikipedia.org/wiki/Left_shift_(medicine)
See also
Blood shift
Leukocytosis
Band cell
Reticulocyte
------------------------
mycosis: blastomycota cota cotic opithsokont kont Zoosporia Opisthokonta Rozellomyceta Chytridiomycota Blastocladiomycota Entomophthoromycota
Mucoromycota
Glomeromycota
Entorrhizomycota
Basidiomycota
Ascomycota
https://en.wikipedia.org/wiki/Fungus
Sepsis is a life-threatening condition that arises when the body's response to infection causes injury to its own tissues and organs.[5] This initial stage is followed by suppression of the immune system.[9]Common signs and symptoms include fever, increased heart rate, increased breathing rate, and confusion.[2] There may also be symptoms related to a specific infection, such as a cough with pneumonia, or painful urination with a kidney infection.[3] The very young, old, and people with a weakened immune system may have no symptoms of a specific infection, and the body temperature may be low or normal instead of having a fever.[3] Severe sepsis causes poor organ function or blood flow.[10] The presence of low blood pressure, high blood lactate, or low urine output may suggest poor blood flow.[10] Septic shock is low blood pressure due to sepsis that does not improve after fluid replacement.[10]
In addition to symptoms related to the actual cause, people with sepsis may have a fever, low body temperature, rapid breathing, a fast heart rate, confusion, and edema.[19] Early signs include a rapid heart rate, decreased urination, and high blood sugar. Signs of established sepsis include confusion, metabolic acidosis (which may be accompanied by a faster breathing rate that leads to respiratory alkalosis), low blood pressure due to decreased systemic vascular resistance, higher cardiac output, and disorders in blood-clotting that may lead to organ failure.[20] Fever is the most common presenting symptom in sepsis, but fever may be absent in some people such as the elderly or those who are immunocompromised.[21]
The drop in blood pressure seen in sepsis can cause lightheadedness and is part of the criteria for septic shock.[22]
Oxidative stress is observed in septic shock, with circulating levels of copper and vitamin C being decreased.[23]
Cause[edit]
Infections leading to sepsis are usually bacterial but may be fungal, parasitic or viral.[24] Gram-positive bacteria were the primary cause of sepsis before the introduction of antibiotics in the 1950s. After the introduction of antibiotics, gram-negative bacteria became the predominant cause of sepsis from the 1960s to the 1980s.[25] After the 1980s, gram-positive bacteria, most commonly staphylococci, are thought to cause more than 50% of cases of sepsis.[8][26] Other commonly implicated bacteria include Streptococcus pyogenes, Escherichia coli, Pseudomonas aeruginosa, and Klebsiella species.[27]Fungal sepsis accounts for approximately 5% of severe sepsis and septic shock cases; the most common cause of fungal sepsis is an infection by Candida species of yeast,[28] a frequent hospital-acquired infection. The most common causes for parasitic sepsis are Plasmodium (which leads to malaria), Schistostoma and Echinococcus.
The most common sites of infection resulting in severe sepsis are the lungs, the abdomen, and the urinary tract.[24] Typically, 50% of all sepsis cases start as an infection in the lungs. In one-third to one-half of cases, the source of infection is unclear.[24]
Systemic inflammatory response syndrome[32] FindingValueTemperature<36 °C (96.8 °F) or >38 °C (100.4 °F)Heart rate>90/minRespiratory rate>20/min or PaCO2<32 mmHg (4.3 kPa)WBC<4x109/L (<4000/mm3), >12x109/L (>12,000/mm3), or ≥10% bands
In 2016 a new consensus was reached to replace screening by systemic inflammatory response syndrome (SIRS) with the sequential organ failure assessment (SOFA score) and the abbreviated version (qSOFA).[5]
The term "σήψις" (sepsis) was introduced by Hippocrates in the fourth century BC, and it meant the process of decay or decomposition of organic matter.[106][107][108] In the eleventh century, Avicenna used the term "blood rot" for diseases linked to severe purulent process. Though severe systemic toxicity had already been observed, it was only in the 19th century that the specific term – sepsis – was used for this condition.
The terms "septicemia", also spelled "septicaemia", and "blood poisoning" referred to the microorganisms or their toxins in the blood. The International Statistical Classification of Diseases and Related Health Problems (ICD) version 9, which was in use in the US until 2013, used the term septicemia with numerous modifiers for different diagnoses, such as "Streptococcal septicemia".[109] All those diagnoses have been converted to sepsis, again with modifiers, in ICD-10, such as "Sepsis due to streptococcus".[109]
The current terms are dependent on the microorganism that is present: bacteremia if bacteria are present in the blood at abnormal levels and are the causative issue, viremia for viruses, and fungemia for a fungus.[110]
The bacteria Streptococcus pneumoniae, Escherichia coli, Proteus spp., Pseudomonas aeruginosa, Staphylococcus aureus, Klebsiella spp., Clostridium spp., Lactobacillus spp., Bacteroides spp. and the fungi Candida spp. are all capable of such a high level of phenotypic plasticity. Evidently, not all cases of sepsis arise through such adaptive microbial strategy switches.[127]
/ˈsɛpsɪs/
Specialty Infectious disease
Symptoms Fever, increased heart rate, low blood pressure, increased breathing rate, confusion[2]
Causes Immune response triggered by an infection[3][4]
Risk factors Young or old age, cancer, diabetes, major trauma, burns[2]
Diagnostic method Systemic inflammatory response syndrome (SIRS),[3] qSOFA[5]
Treatment Intravenous fluids, antimicrobials[2][6]
Prognosis 10 to 80% risk of death[5][7]
Frequency 0.2–3 per 1000 a year (developed world)[7][8]
End-organ dysfunction[edit]
Main article: Multiple organ dysfunction syndrome
Examples of end-organ dysfunction include the following:[37]
Lungs: acute respiratory distress syndrome (ARDS) (PaO2/FiO2 ratio< 300), different ratio in pediatric acute respiratory distress syndrome
Brain: encephalopathy symptoms including agitation, confusion, coma; causes may include ischemia, bleeding, formation of blood clots in small blood vessels, microabscesses, multifocal necrotizing leukoencephalopathy
Liver: disruption of protein synthetic function manifests acutely as progressive disruption of blood clotting due to an inability to synthesize clotting factors and disruption of metabolic functions leads to impaired bilirubin metabolism, resulting in elevated unconjugated serum bilirubin levels
Kidney: low urine output or no urine output, electrolyte abnormalities, or volume overload
Heart: systolic and diastolic heart failure, likely due to chemical signals that depress myocyte function, cellular damage, manifest as a troponin leak (although not necessarily ischemic in nature)
More specific definitions of end-organ dysfunction exist for SIRS in pediatrics.[38]
Cardiovascular dysfunction (after fluid resuscitation with at least 40 ml/kg of crystalloid)
hypotension with blood pressure < 5th percentile for age or systolic blood pressure < 2 standard deviations below normal for age, or
vasopressor requirement, or
two of the following criteria:
unexplained metabolic acidosis with base deficit > 5 mEq/l
lactic acidosis: serum lactate 2 times the upper limit of normal
oliguria (urine output < 0.5 ml/kg/h)
prolonged capillary refill > 5 seconds
core to peripheral temperature difference > 3 °C
Respiratory dysfunction (in the absence of a cyanotic heart defect or a known chronic respiratory disease)
the ratio of the arterial partial-pressure of oxygen to the fraction of oxygen in the gases inspired (PaO2/FiO2) < 300 (the definition of acute lung injury), or
arterial partial-pressure of carbon dioxide (PaCO2) > 65 torr (20 mmHg) over baseline PaCO2 (evidence of hypercapnic respiratory failure), or
supplemental oxygen requirement of greater than FiO2 0.5 to maintain oxygen saturation ≥ 92%
Neurologic dysfunction
Glasgow Coma Score (GCS) ≤ 11, or
altered mental status with drop in GCS of 3 or more points in a person with developmental delay/intellectual disability
Hematologic dysfunction
platelet count < 80,000/mm3 or 50% drop from maximum in chronically thrombocytopenic, or
international normalized ratio (INR) > 2
Disseminated intravascular coagulation
Kidney dysfunction
serum creatinine ≥ 2 times the upper limit of normal for age or 2-fold increase in baseline creatinine in people with chronic kidney disease
Liver dysfunction (only applicable to infants > 1 month)
total serum bilirubin ≥ 4 mg/dl, or
alanine aminotransferase (ALT) ≥ 2 times the upper limit of normal
Consensus definitions, however, continue to evolve, with the latest expanding the list of signs and symptoms of sepsis to reflect clinical bedside experience.[19]
Biomarkers[edit]
A 2013 review concluded moderate-quality evidence exists to support the use of the procalcitonin level as a method to distinguish sepsis from non-infectious causes of SIRS.[30] The same review found the sensitivity of the test to be 77% and the specificity to be 79%. The authors suggested that procalcitonin may serve as a helpful diagnostic marker for sepsis, but cautioned that its level alone does not definitively make the diagnosis.[30] A 2012 systematic review found that soluble urokinase-type plasminogen activator receptor (SuPAR) is a nonspecific marker of inflammation and does not accurately diagnose sepsis.[39] This same review concluded, however, that SuPAR has prognostic value, as higher SuPAR levels are associated with an increased rate of death in those with sepsis.[39] Serial measurement of lactate levels (approximately every 4 to 6 hours) may guide treatment and is associated with lower mortality in sepsis.[21]
Differential diagnosis[edit]
The differential diagnosis for sepsis is broad and has to examine (to exclude) the non-infectious conditions that may cause the systemic signs of SIRS: alcohol withdrawal, acute pancreatitis, burns, pulmonary embolism, thyrotoxicosis, anaphylaxis, adrenal insufficiency, and neurogenic shock.[20][40]Hyperinflammatory syndromes such as hemophagocytic lymphohistiocytosis (HLH) may have similar symptoms and are on the differential diagnosis.[41]
In common clinical usage, neonatal sepsis refers to a bacterial blood stream infection in the first month of life, such as meningitis, pneumonia, pyelonephritis, or gastroenteritis,[42] but neonatal sepsis also may be due to infection with fungi, viruses, or parasites.[42] Criteria with regard to hemodynamic compromise or respiratory failure are not useful because they present too late for intervention.
Pathophysiology[edit]
This section needs expansionwith: Viral sepsis. You can help by adding to it. (March 2020)
Sepsis is caused by a combination of factors related to the particular invading pathogen(s) and to the status of the immune system of the host.[43] The early phase of sepsis characterized by excessive inflammation (sometimes resulting in a cytokine storm) may be followed by a prolonged period of decreased functioning of the immune system.[44][9] Either of these phases may prove fatal. On the other hand, systemic inflammatory response syndrome (SIRS) occurs in people without the presence of infection, for example, in those with burns, polytrauma, or the initial state in pancreatitis and ...However, sepsis also causes similar response to SIRS.[18]
Microbial factors[edit]
Bacterial virulence factors, such as glycocalyx and various adhesins, allow colonization, immune evasion, and establishment of disease in the host.[43]Sepsis caused by gram-negative bacteria is thought to be largely due to a response by the host to the lipid A component of lipopolysaccharide, also called endotoxin.[45][46] Sepsis caused by gram-positive bacteria may result from an immunological response to cell wall lipoteichoic acid.[47] Bacterial exotoxinsthat act as superantigens also may cause sepsis.[43] Superantigens simultaneously bind major histocompatibility complex and T-cell receptors in the absence of antigen presentation. This forced receptor interaction induces the production of pro-inflammatory chemical signals (cytokines) by T-cells.[43]
There are a number of microbial factors that may cause the typical septic inflammatory cascade. An invading pathogen is recognized by its pathogen-associated molecular patterns (PAMPs). Examples of PAMPs include lipopolysaccharides and flagellin in gram-negative bacteria, muramyl dipeptide in the peptidoglycan of the gram-positive bacterial cell wall, and CpG bacterial DNA. These PAMPs are recognized by the pattern recognition receptors (PRRs) of the innate immune system, which may be membrane-bound or cytosolic.[48] There are four families of PRRs: the toll-like receptors, the C-type lectinreceptors, the NOD-like receptors, and the RIG-I-like receptors. Invariably, the association of a PAMP and a PRR will cause a series of intracellular signalling cascades. Consequentially, transcription factors such as nuclear factor-kappa B and activator protein-1, will up-regulate the expression of pro-inflammatory and anti-inflammatory cytokines.[49]
Meanwhile, in the heart, impaired calcium transport, and low production of adenosine triphosphate (ATP), can cause myocardial depression, reducing cardiac contractility and causing heart failure.
Cytokines such as tumor necrosis factor, interleukin 1, and interleukin 6 may activate procoagulation factors in the cells lining blood vessels, leading to endothelial damage. The damaged endothelial surface inhibits anticoagulant properties as well as increases antifibrinolysis, which may lead to intravascular clotting, the formation of blood clots in small blood vessels, and multiple organ failure.[52]
The low blood pressure seen in those with sepsis is the result of various processes, including excessive production of chemicals that dilate blood vesselssuch as nitric oxide, a deficiency of constriction integrity of blood vasculature (constriction dependent function ; forces/env dist/etc. struct aberrat becom dysf) [electrocution; radK; ionization/particularization/nuclear/waveform/gradient change/change/energy state change/matrix change/intercal change/polarity change/flux/flow interruption/etc. weaps; distance incapacitation weapon; induction of protein dimers by signal/weapon; bacter lysis by signal/weapon, time, trigger, force, etc.; etc.] of chemicals that constrict blood vessels such as vasopressin, and activation of ATP-sensitive potassium channels.[53] In those with severe sepsis and septic shock, this sequence of events leads to a type of circulatory shock known as distributive shock.[54]
https://en.wikipedia.org/wiki/Sepsis
Fungemia is the presence of fungi or yeasts in the blood. The most common type, also known as candidemia, candedemia, or systemic candidiasis, is caused by Candida species; candidemia is also among the most common bloodstream infections of any kind.[1] Infections by other fungi, including Saccharomyces, Aspergillus and Cryptococcus, are also called fungemia. It is most commonly seen in immunosuppressed or immunocompromised patients with severe neutropenia, cancer patients, or in patients with intravenous catheters. It has been suggested the otherwise immunocompetent patients taking infliximab may be at a higher risk for fungemia.
Diagnosis is difficult, as routine blood cultures have poor sensitivity.[2]
https://en.wikipedia.org/wiki/Fungemia
Viremia is a medical condition where viruses enter the bloodstream and hence have access to the rest of the body. It is similar to bacteremia, a condition where bacteria enter the bloodstream.[1] The name comes from combining the word "virus" with the Greek word for "blood" (haima). It usually lasts for 4 to 5 days in the primary condition.
https://en.wikipedia.org/wiki/Viremia
Bloodstream infections (BSIs), which include bacteremias when the infections are bacterial and fungemias when the infections are fungal, are infections present in the blood.[1] Blood is normally a sterileenvironment,[2] so the detection of microbes in the blood (most commonly accomplished by blood cultures[3]) is always abnormal. A bloodstream infection is different from sepsis, which is the host response to bacteria.[4]
Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including during intravenous drug abuse).[5] Transient bacteremia can result after dental procedures or brushing of teeth.[6]
Bacteremia can have several important health consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate.[7] Bacteria can also spread via the blood to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection, such as endocarditis or osteomyelitis.[citation needed] Treatment for bacteremia is with antibiotics, and prevention with antibiotic prophylaxis can be given in high risk situations.[8]
https://en.wikipedia.org/wiki/Bloodstream_infections
Critical green inclusions, also known as green neutrophilic inclusions and informally, death crystals or crystals of death,[1][2] are amorphous blue-green cytoplasmic inclusions found in neutrophils and occasionally in monocytes. They appear brightly coloured and refractile when stained with Wright-Giemsa stain. These inclusions are most commonly found in critically ill patients, particularly those with liver disease, and their presence on the peripheral blood smear is associated with a high short-term mortality rate.[3][4]
https://en.wikipedia.org/wiki/Critical_green_inclusion#cite_note-ACLS2017-4
Jordans' anomaly (also known as Jordan anomaly and Jordans bodies) is a familial abnormality of white blood cell morphology. Individuals with this condition exhibit persistent vacuolation of granulocytes and monocytes in the peripheral blood and bone marrow. Jordans' anomaly is associated with neutral lipid storage diseases.[1][2][3]
https://en.wikipedia.org/wiki/Jordans%27_anomaly
Auer rods (or Auer bodies) are large, crystalline cytoplasmic inclusion bodies sometimes observed in myeloidblast cells during acute myeloid leukemia, acute promyelocytic leukemia, and high-grade myelodysplastic syndromes and myeloproliferative disorders. Composed of fused lysosomes and rich in lysosomal enzymes, Auer rods are azurophilic and can resemble needles, commas, diamonds, rectangles, corkscrews, or rarely granules.[1]
Systemic inflammatory response syndrome (SIRS), is an inflammatory state affecting the whole body.[1] It is the body's response to an infectious or noninfectious insult. Although the definition of SIRS refers to it as an "inflammatory" response, it actually has pro- and anti-inflammatory components.
https://en.wikipedia.org/wiki/Systemic_inflammatory_response_syndrome
The sequential organ failure assessment score (SOFA score), previously known as the sepsis-related organ failure assessment score,[1] is used to track a person's status during the stay in an intensive care unit (ICU) to determine the extent of a person's organ function or rate of failure.[2][3][4][5][6] The score is based on six different scores, one each for the respiratory, cardiovascular, hepatic, coagulation, renal and neurological systems.
The score tables below only describe points-giving conditions. In cases where the physiological parameters do not match any row, zero points are given. In cases where the physiological parameters match more than one row, the row with most points is picked.
The quick SOFA score (qSOFA) assists health care providers in estimating the risk of morbidity and mortality due to sepsis.[7]
Quick SOFA score[edit]
The Quick SOFA Score (quickSOFA or qSOFA) was introduced by the Sepsis-3 group in February 2016 as a simplified version of the SOFA Score as an initial way to identify patients at high risk for poor outcome with an infection.[11] The SIRS Criteria definitions of sepsis are being replaced as they were found to possess too many limitations; the "current use of 2 or more SIRS criteria to identify sepsis was unanimously considered by the task force to be unhelpful." The qSOFA simplifies the SOFA score drastically by only including its 3 clinical criteria and by including "any altered mentation" instead of requiring a GCS <15. qSOFA can easily and quickly be repeated serially on patients.
| Assessment | qSOFA score |
|---|---|
| Low blood pressure (SBP ≤ 100 mmHg) | 1 |
| High respiratory rate (≥ 22 breaths/min) | 1 |
| Altered mentation (GCS ≤ 14) | 1 |
The score ranges from 0 to 3 points. The presence of 2 or more qSOFA points near the onset of infection was associated with a greater risk of death or prolonged intensive care unit stay. These are outcomes that are more common in infected patients who may be septic than those with uncomplicated infection. Based upon these findings, the Third International Consensus Definitions for Sepsis recommends qSOFA as a simple prompt to identify infected patients outside the ICU who are likely to be septic.[12]
https://en.wikipedia.org/wiki/SOFA_score#Quick_SOFA_score
Multiple organ dysfunction syndrome (MODS) is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.
Although Irwin and Rippe cautioned in 2005 that the use of "multiple organ failure" or "multisystem organ failure" should be avoided,[1] both Harrison's (2015) and Cecil's (2012) medical textbooks still use the terms "multi-organ failure" and "multiple organ failure" in several chapters and do not use "multiple organ dysfunction syndrome" at all.
| Multiple organ dysfunction syndrome | |
|---|---|
| Other names | Total organ failure, multisystem organ failure, multiple organ failure |
| Causes | Infection, injury, hypermetabolism |
| Prognosis | Case fatality rate 30%-100% depending on the number of organs that failed |
Endotoxin macrophage hypothesis[edit]
Gram-negative infections in MODS patients are relatively common, hence endotoxins have been advanced as principal mediator in this disorder. It is thought that following the initial event cytokines are produced and released. The pro-inflammatory mediators are: tumor necrosis factor-alpha (TNF-α), interleukin-1, interleukin-6, thromboxane A2, prostacyclin, platelet activating factor, and nitric oxide.[1]
Tissue hypoxia-microvascular hypothesis[edit]
As a result of macro- and microvascular changes insufficient supply of oxygen occurs. Hypoxemia causes cell death and organ dysfunction.[1]
Mitochondrial DNA hypothesis[edit]
According to findings of Professor Zsolt Balogh and his team at the University of Newcastle (Australia), mitochondrial DNA is the leading cause of severe inflammation due to a massive amount of mitochondrial DNA that leaks into the bloodstream due to cell death of patients who survived major trauma.[citation needed]
Mitochondrial DNA resembles bacterial DNA. If bacteria triggers leukocytes, mitochondrial DNA may do the same. When confronted with bacteria, white blood cells, or neutrophil granulocytes, behave like predatory spiders. They spit out a web, or net, to trap the invaders, then hit them with a deadly oxidative blast, forming neutrophil extracellular traps (NETs).[citation needed]
This results in catastrophic immune response leading to multiple organ dysfunction syndrome.[4][5]
In patients with sepsis, septic shock, or multiple organ dysfunction syndrome that is due to major trauma, the rs1800625 polymorphism is a functional single nucleotide polymorphism, a part of the receptor for advanced glycation end products (RAGE) transmembrane receptor gene (of the immunoglobulin superfamily) and confers host susceptibility to sepsis and MODS in these patients.[11]
Further reading[edit]
- The ICU Book by Marino
- Cecil Textbook of Medicine
- The Oxford Textbook of Medicine
- Harrison's Principles of Internal Medicine
Acute respiratory distress syndrome (ARDS) is a type of respiratory failure characterized by rapid onset of widespread inflammation in the lungs.[1] Symptoms include shortness of breath (dyspnea), rapid breathing (tachypnea), and bluish skin coloration (cyanosis).[1] For those who survive, a decreased quality of life is common.[3]
Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration.[1] The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting.[4] In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide.[1] Adult diagnosis is based on a PaO2/FiO2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O.[1] Cardiogenic pulmonary edema, as the cause, must be excluded.[3]
The primary treatment involves mechanical ventilation together with treatments directed at the underlying cause.[1] Ventilation strategies include using low volumes and low pressures.[1] If oxygenation remains insufficient, lung recruitment maneuvers and neuromuscular blockers may be used.[1] If these are insufficient, extracorporeal membrane oxygenation (ECMO) may be an option.[1]The syndrome is associated with a death rate between 35 and 50%.[1]
Globally, ARDS affects more than 3 million people a year.[1] The condition was first described in 1967.[1] Although the terminology of "adult respiratory distress syndrome" has at times been used to differentiate ARDS from "infant respiratory distress syndrome" in newborns, the international consensus is that "acute respiratory distress syndrome" is the best term because ARDS can affect people of all ages.[5] There are separate diagnostic criteria for children and those in areas of the world with fewer resources.[3]
https://en.wikipedia.org/wiki/Acute_respiratory_distress_syndrome
Blood film findings
Red blood cells
Size
Anisocytosis
Macrocytosis
Microcytosis
Shape
Poikilocytosis
Membrane abnormalities
Acanthocyte
Codocyte
Elliptocyte
Hereditary elliptocytosis
Spherocyte
Hereditary spherocytosis
Dacrocyte
Echinocyte
Schistocyte
Degmacyte
Sickle cell/drepanocyte
Sickle cell disease
Stomatocyte
Hereditary stomatocytosis
Colour
Anisochromia
Hypochromic anemia
Polychromasia
Inclusion bodies
Developmental
Howell–Jolly body
Basophilic stippling
Pappenheimer bodies
Cabot rings
Hemoglobin precipitation
Heinz body
Other
Red cell agglutination
Rouleaux
White blood cells
Lymphocytes
Reactive lymphocyte
Smudge cell
Russell bodies
Granulocytes
Hypersegmented neutrophil
Arneth count
Pelger–Huët anomaly
Döhle bodies
Toxic granulation
Toxic vacuolation
Critical green inclusion
Alder–Reilly anomaly
Jordans' anomaly
Left shift
Other
Auer rod
Categories:
Sepsis
Infectious diseases
Intensive care medicine
Medical emergencies
Neonatology
show
Authority control
https://en.wikipedia.org/wiki/Sepsis
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