Lymphangitis is an inflammation or an infection of the lymphatic channels that occurs as a result of infection at a site distal to the channel. The most common cause of lymphangitis in humans is "Streptococcus pyogenes" (Group A strep), although it can also be caused by the fungus "Sporothrix schenckii". Lymphangitis is sometimes mistakenly called "blood poisoning". In reality, "blood poisoning" is synonymous with "sepsis".

Signs and symptoms include a deep reddening of the skin, warmth, lymphadenitis (inflammation of a lymphatic gland), and a raised border around the affected area. The person may also have chills and a high fever along with moderate pain and swelling. A person with lymphangitis should be hospitalized and closely monitored by medical professionals.

Lymphangitis is the inflammation of the lymphatic vessels and channels. This is characterized by certain inflammatory conditions of the skin caused by bacterial infections. Thin red lines may be observed running along the course of the lymphatic vessels in the affected area, accompanied by painful enlargement of the nearby lymph nodes.

When the inferior limbs are affected, the redness of the skin runs over the great saphenous vein location and confusion can be made with a thrombophlebitis.

Chronic lymphangitis is a cutaneous condition that is the result of recurrent bouts of acute bacterial lymphangitis.

Hematemesis or haematemesis is the vomiting of blood. The source is generally the upper gastrointestinal tract, typically above the suspensory muscle of duodenum. Patients can easily confuse it with hemoptysis (coughing up blood), although the latter is more common. Hematemesis "is always an important sign".

Causes can be:

- Mallory-Weiss syndrome: bleeding tears in the esophagal mucosa, usually caused by prolonged and vigorous retching.

- Irritation or erosion of the lining of the esophagus or stomach

- Vomiting of ingested blood after hemorrhage in the oral cavity, nose or throat

- Vascular malfunctions of the gastrointestinal tract, such as bleeding gastric varices or intestinal varices

- Tumors of the stomach or esophagus.

- Radiation poisoning

- Viral hemorrhagic fevers

- Gastroenteritis

- Gastritis

- Peptic ulcer

- Chronic viral hepatitis

- Intestinal schistosomiasis (caused by the parasite "Schistosoma mansoni")

- History of smoking

- Iatrogenic injury (invasive procedure such as endoscopy or transesophageal echocardiography)

- Zollinger–Ellison syndrome (severe peptic ulcer)

- Atrio-oesophageal fistula

- Yellow fever

Aspirin overdose has potentially serious consequences, sometimes leading to significant morbidity and death. Patients with mild intoxication frequently have nausea and vomiting, abdominal pain, lethargy, ringing in the ears, and dizziness. More significant signs and symptoms occur in more severe poisonings and include high body temperature, fast breathing rate, respiratory alkalosis, metabolic acidosis, low blood potassium, low blood glucose, hallucinations, confusion, seizure, cerebral edema, and coma. The most common cause of death following an aspirin overdose is cardiopulmonary arrest usually due to pulmonary edema.

After ingestion, toxic features usually develop within a few minutes. The major lethal consequence of aluminium phosphide ingestion is profound circulatory collapse, and is reportedly secondary to these toxins generated, which lead due to direct effects on cardiomyocytes, fluid loss, and adrenal gland damage. The signs and symptoms are non-specific, dose dependent and evolve with time passing. The dominant clinical feature is severe hypotension refractory to dopamine therapy. Other features may include dizziness, fatigue, tightness in the chest, headache, nausea, vomiting, diarrhoea, ataxia, numbness, paraesthesia, tremor, muscle weakness, diplopia and jaundice. If severe inhalation occurs, the patient may develop acute respiratory distress syndrome (ARDS), heart failure, arrhythmias, convulsion and coma. Late manifestation include liver and kidney toxicities.

The diagnosis of AAlP usually depends on the clinical suspicion or history (self-report or by attendants). In some nations, tablets of AlP are also referred to as "rice tablets" and, if there is a history of rice tablet ingestion, then it should be treated differently from other types of rice tablets that are made up of herbal products. For a silver nitrate test on gastric aspirate, diluted gastric content can be positive.

The signs and symptoms of paracetamol toxicity occur in three phases. The first phase begins within hours of overdose, and consists of nausea, vomiting, a pale appearance, and sweating. However, patients often have no specific symptoms or only mild symptoms in the first 24 hours of poisoning. Rarely, after massive overdoses, patients may develop symptoms of metabolic acidosis and coma early in the course of poisoning.

The second phase occurs between 24 h and 72 h following overdose and consists of signs of increasing liver damage. In general, damage occurs in liver cells as they metabolize the paracetamol. The individual may experience right upper quadrant abdominal pain. The increasing liver damage also changes biochemical markers of liver function; International normalized ratio (INR) and the liver transaminases ALT and AST rise to abnormal levels. Acute kidney failure may also occur during this phase, typically caused by either hepatorenal syndrome or multiple organ dysfunction syndrome. In some cases, acute kidney failure may be the primary clinical manifestation of toxicity. In these cases, it has been suggested that the toxic metabolite is produced more in the kidneys than in the liver.

The third phase follows at 3 to 5 days, and is marked by complications of massive liver necrosis leading to fulminant liver failure with complications of coagulation defects, low blood sugar, kidney failure, hepatic encephalopathy, brain swelling, sepsis, multiple organ failure, and death. If the third phase is survived, the liver necrosis runs its course, and liver and kidney function typically return to normal in a few weeks. The severity of paracetamol toxicity varies depending on the dose and whether appropriate treatment is received.

In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning.

Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor and/or lividity is another feature. A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders. Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.

Digoxin toxicity is often divided into acute or chronic toxicity. In both of these toxicity, cardiac effects are of the greatest concern. With an acute ingestion, symptoms such as nausea, vertigo, and vomiting are prominent. On the other hand, nonspecific symptoms are more predominate in chronic toxicity. These symptoms include fatigue, malaise, and visual disturbances.

The classic features of digoxin toxicity are nausea, vomiting, abdominal pain, headache, dizziness, confusion, delirium, vision disturbance (blurred or yellow vision). It is also associated with cardiac disturbances including irregular heartbeat, ventricular tachycardia, ventricular fibrillation, sinoatrial block and AV block.

The main manifestations of carbon monoxide poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart. The initial symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue. These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis. Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous. Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia; central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and death. Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney failure, skin lesions, and visual and auditory problems.

One of the major concerns following acute carbon monoxide poisoning is the severe delayed neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like syndromes, cortical blindness, and a depressed mood. Depression may occur in those who did not have pre-existing depression. These delayed neurological sequelae may occur in up to 50% of poisoned people after 2 to 40 days. It is difficult to predict who will develop delayed sequelae; however, advanced age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.

One classic sign of carbon monoxide poisoning is more often seen in the dead rather than the living – people have been described as looking red-cheeked and healthy (see below). However, since this "cherry-red" appearance is common only in the deceased, and is unusual in living people, it is not considered a useful diagnostic sign in clinical medicine. In pathological (autopsy) examination the ruddy appearance of carbon monoxide poisoning is notable because unembalmed dead persons are normally bluish and pale, whereas dead carbon-monoxide poisoned persons may simply appear unusually lifelike in coloration. The colorant effect of carbon monoxide in such postmortem circumstances is thus analogous to its use as a red colorant in the commercial meat-packing industry.

Acute aluminium phosphide poisoning (AAlPP) is a large, though under-reported, problem throughout the world, particularly in the Indian subcontinent. Aluminium phosphide (AlP), which is readily available as a fumigant for stored cereal grains, sold under various brand names such as "QuickPhos" and "Celphos", is highly toxic, especially when consumed from a freshly opened container. Death results from profound shock, myocarditis and multi-organ failure. Aluminium phosphide has a fatal dose of between . It has been reported to be the most common cause of suicidal death in North India. Deaths have also been reported in Iran. In January 2017, four children died at a trailer park in Amarillo, Texas, after the pesticide was used under the home to kill rats. Several incidents of death in travelers in Thailand and other parts of Southeast Asia may have been caused by aluminum phosphide or chlorpyrifos, an organophosphate insecticide, used in an attempt to kill bedbugs in hotels. Wired magazine reported on the problem in March 2014. A short film in Arabic on Youtube that focused on the problem in Saudi Arabia had over 3.5 million hits in 2014. The CDC has classified phosphine as immediately dangerous to life at 50 parts per million.

Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. This may include feeling tired, abdominal pain, or nausea. This is typically followed by a couple of days without any symptoms after which yellowish skin, blood clotting problems, and confusion occurs. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment some cases will resolve while others will result in death.

Paracetamol poisoning can occur accidentally or as an attempt to end one's life. Risk factors for toxicity include alcoholism, malnutrition, and the taking of certain other medications. Liver damage results not from paracetamol itself, but from one of its metabolites, "N"-acetyl-"p"-benzoquinone imine (NAPQI). NAPQI decreases the liver's glutathione and directly damages cells in the liver. Diagnosis is based on the blood level of paracetamol at specific times after the medication was taken. These values are often plotted on the Rumack-Matthew nomogram to determine level of concern.

Treatment may include activated charcoal if the person presents soon after the overdose. Attempting to force the person to vomit is not recommended. If there is a potential for toxicity, the antidote acetylcysteine is recommended. The medication is generally given for at least 24 hours. Psychiatric care may be required following recovery. A liver transplant may be required if damage to the liver becomes severe. The need for transplant is often based on low blood pH, high blood lactate, poor blood clotting, or significant hepatic encephalopathy. With early treatment liver failure is rare. Death occurs in about 0.1% of cases.

Paracetamol poisoning was first described in the 1960s. Rates of poisoning vary significantly between regions of the world. In the United States more than 100,000 cases occur a year. In the United Kingdom it is the medication responsible for the greatest number of overdoses. Young children are most commonly affected. In the United States and the United Kingdom paracetamol is the most common cause of acute liver failure.

Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. Early on these may be subtle while larger doses may result in fever. Complications can include swelling of the brain or lungs, seizures, low blood sugar, or cardiac arrest.

While usually due to aspirin, other possible causes include oil of wintergreen and bismuth subsalicylate. Excess doses can be either on purpose or accidental. Small amounts of oil of wintergreen can be toxic. Diagnosis is generally based on repeated blood tests measuring aspirin levels and blood gases. While a type of graph has been created to try to assist with diagnosis, its general use is not recommended. In overdose maximum blood levels may not occur for more than 12 hours.

Efforts to prevent poisoning include child-resistant packaging and a lower number of pills per package. Treatment may include activated charcoal, intravenous sodium bicarbonate with dextrose and potassium chloride, and dialysis. Giving dextrose may be useful even if the blood sugar is normal. Dialysis is recommended in those with kidney failure, decreased level of consciousness, blood pH less than 7.2, or high blood salicylate levels. If a person requires intubation a fast respiratory rate may be required.

The toxic effects of salicylates have been described since at least 1877. In 2004 more than 20,000 cases with 43 deaths were reported in the United States. About 1% of those with an acute overdose die while chronic overdoses may have worse outcomes. Older people are at higher risks of toxicity for any given dose.

The first signs of poisoning suggest an allergic reaction with the following symptoms:

- facial flushing/sweating

- burning-peppery taste sensations in the mouth and throat

- dizziness

- nausea

- headache

- tachycardia

- cold-like symptoms

The above symptoms can advance to:

- facial rash (intense itching may accompany the rash.)

- torso or body rash: The rash associated with scombroid poisoning is a form of urticaria, but most commonly does not include wheals (patchy areas of skin-swelling also known as hives) that may be seen in true allergies.

- edema (this is generalized if it occurs at all)

- short-term diarrhea

- abdominal cramps

Epidemic dropsy is a form of edema of extremities due to poisoning by "Argemone mexicana" (Mexican prickly poppy).

Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with "Argemone mexicana" seed oil.

Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.

Other major symptoms are pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.

Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.

Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.

Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica "juncea" commonly known as Indian mustard ) as cooking medium is common.

In individuals with suspected digoxin toxicity, a serum digoxin concentration, serum potassium concentration, creatinine, BUN, and serial electrocardiograms is obtained.

Hematochezia is the passage of fresh blood through the anus, usually in or with stools (contrast with melena). Hematochezia is commonly associated with lower gastrointestinal bleeding, but may also occur from a brisk upper gastrointestinal bleed. The difference between hematochezia and rectorrhagia is that, in the latter, rectal bleeding is not associated with defecation; instead, it is associated with expulsion of fresh bright red blood without stools. The phrase bright red blood per rectum (BRBPR) is associated with hematochezia and rectorrhagia. It is also important to differentiate from hematopapyrus - blood on the toilet paper noticed when wiping. The term is from Greek αἷμα ("blood") and χέζειν ("to defaecate").

The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain's oxygen needs then no symptoms will result.

However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory. If oxygen deprivation continues, cognitive disturbances, and decreased motor control will result. The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death.

Objective measurements of the severity of cerebral hypoxia depend on the cause. Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. In hypoxic hypoxia 95–100% saturation is considered normal; 91–94% is considered mild and 86–90% moderate. Anything below 86% is considered severe.

It should be noted that cerebral hypoxia refers to oxygen levels in brain tissue, not blood. Blood oxygenation will usually appear normal in cases of hypemic, ischemic, and hystoxic cerebral hypoxia. Even in hypoxic hypoxia blood measures are only an approximate guide; the oxygen level in the brain tissue will depend on how the body deals with the reduced oxygen content of the blood.

Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock. It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

- Transient ischemic attack (TIA), is often referred to as a "mini-stroke". The American Heart Association and American Stroke Association (AHA/ASA) refined the definition of transient ischemic attack. TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The symptoms of a TIA can resolve within a few minutes, unlike a stroke. TIAs share the same underlying etiology as strokes; a disruption of cerebral blood flow. TIAs and strokes present with the same symptoms such as contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech, and mental confusion. The symptoms of a TIA typically resolve within 24 hours, unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke.

- Silent stroke is a stroke which does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. Despite its lack of identifiable symptoms, a silent stroke still causes brain damage and places the patient at increased risk for a major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as fMRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being predisposing factors.

Carbon monoxide is not toxic to all forms of life. Its harmful effects are due to binding with hemoglobin so its danger to organisms that do not use this compound is doubtful. It thus has no effect on photosynthesising plants. It is easily absorbed through the lungs. Inhaling the gas can lead to hypoxic injury, nervous system damage, and even death. Different people and populations may have different carbon monoxide tolerance levels. On average, exposures at 100 ppm or greater is dangerous to human health. In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period; in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached. Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage. The carbon monoxide tolerance level for any person is altered by several factors, including activity level, rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other hematological disorders, barometric pressure, and metabolic rate.

Signs of ethylene glycol poisoning depend upon the time after ingestion. Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.

- Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning. Poisoned individuals may appear to be intoxicated, dizzy, lacking coordination of muscle movements, drooling, depressed, and have slurred speech, seizuring, abnormal eye movements, headaches, and confusion. Irritation to the stomach may cause nausea and vomiting. Also seen are excessive thirst and urination. Over time, the body metabolizes ethylene glycol into other toxins.

- Stage 2 (12 to 36 hours) where signs of "alcohol" poisoning appear to resolve, underlying severe internal damage is still occurring. An elevated heart rate, hyperventilation or increased breathing effort, and dehydration may start to develop, along with high blood pressure and metabolic acidosis. These symptoms are a result of accumulation of organic acids formed by the metabolism of ethylene glycol. Additionally low calcium concentrations in the blood, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If untreated, death most commonly occurs during this period.

- Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze. During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetance may be seen. Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure. If kidney failure occurs it is typically reversible, although weeks or months of supportive care including hemodialysis may be required before kidney function returns.

In adults, most common causes are hemorrhoids and diverticulosis, both of which are relatively benign; however, it can also be caused by colorectal cancer, which is potentially fatal. In a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an initial symptom of necrotizing enterocolitis, a serious condition affecting premature infants. In babies, haematochezia in conjunction with abdominal pain is associated with intussusception. In adolescents and young adults, inflammatory bowel disease, particularly ulcerative colitis, is a serious cause of haematochezia that must be considered and excluded.

Hematochezia can be due to upper gastrointestinal bleeding. However, as the blood from such a bleed is usually chemically modified by action of acid and enzymes, it presents more commonly as black "tarry" feces known as melena. Haematochezia from an upper gastrointestinal source is an ominous sign, as it suggests a very significant bleed which is more likely to be life-threatening.

Beeturia can cause red colored feces after eating beets because of insufficient metabolism of a red pigment, and is a differential sign that may be mistaken as hematochezia.

Consumption of dragon fruit or pitaya may also cause red discoloration of the stool and sometimes the urine (pseudohematuria). This too, is a differential sign that is sometimes mistaken for hematochezia.

In infants, the Apt test can be used to distinguish fetal hemoglobin from maternal blood.

Other common causes of blood in the stool include:

- Colorectal cancer

- Crohns disease

- Ulcerative colitis

- Other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration

- Rectal or anal hemorrhoids or anal fissures, particularly if they rupture or are otherwise irritated

- "Shigella" or shiga toxin producing "E. coli" food poisoning

- Necrotizing enterocolitis

- Diverticulosis

- Salmonellosis

- Upper gastrointestinal bleeding

- Peptic ulcer disease

- Esophageal varices

- Gastric cancer

- Intense exercise, especially a high-impact activity like running in hot weather.

Pancytopenia usually requires a bone marrow biopsy in order to distinguish among different causes.

- anemia: hemoglobin < 13.5 g/dL (male) or 12 g/dL (female).

- leukopenia: total white cell count < 4.0 x 10/L. Decrease in all types of white blood cells (revealed by doing a differential count).

- thrombocytopenia: platelet count < 150×10/L.

Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as

severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur.

Extreme acidemia leads to neurological and cardiac complications:

- Neurological: lethargy, stupor, coma, seizures

- Cardiac: arrhythmias (ventricular tachycardia) and decreased response to epinephrine, both leading to hypotension

Physical examination occasionally reveals signs of disease, but is otherwise normal. Cranial nerve abnormalities are reported in ethylene glycol poisoning, and retinal edema can be a sign of methanol intoxication. Longstanding chronic metabolic acidosis leads to osteoporosis and can cause fractures.