Most SCLS patients report having flu-like symptoms (like a runny nose), or else gastro-intestinal disorders (diarrhea or vomiting), or a general weakness or pain in their limbs, but others get no particular or consistent warning signs ahead of their episodes. They subsequently develop thirst and lightheadedness and the following conditions measurable in a hospital emergency-room setting:

- hemoconcentration (elevated hematocrit or hemoglobin readings, with hematocrit levels >49% in men and >43% in women, not because of an absolute increase in them but because of the leak of plasma);

- very low blood pressure (profound arterial hypotension, with systolic blood pressure levels <90 mm Hg);

- albumin deficiency (hypoalbuminemia measuring <3.0 g/dL);

- partial or generalized edema, and cold extremities;

- a paraprotein in the blood (an MGUS in approximately 80% of cases).

Capillary leak syndrome is characterized by the escape of blood plasma through capillary walls, from the blood circulatory system to surrounding tissues, muscle compartments, organs or body cavities. It is a phenomenon most commonly witnessed in sepsis, and less frequently in autoimmune diseases, differentiation syndrome, engraftment syndrome, hemophagocytic lymphohistiocytosis, the ovarian hyperstimulation syndrome, viral hemorrhagic fevers, and snakebite and ricin poisoning. Pharmaceuticals, including the chemotherapy medication gemcitabine, as well as certain interleukins and monoclonal antibodies, can also cause capillary leaks. These conditions and factors are sources of secondary capillary leak syndrome.

Systemic capillary leak syndrome (SCLS, or Clarkson's disease), or primary capillary leak syndrome, is a rare, grave and episodic medical condition observed largely in otherwise healthy individuals mostly in middle age. It is characterized by self-reversing episodes during which the endothelial cells which line the capillaries, usually of the extremities, separate for one to three days, causing a leakage of plasma mainly into the muscle compartments of the arms and legs. The abdomen, the central nervous system, and the organs (including the lungs) are typically spared, but the extravasation in the extremities is sufficiently massive to cause circulatory shock and compartment syndromes, with a dangerous hypotension (low blood pressure), hemoconcentration(thickening of the blood) and hypoalbuminemia (drop in albumin, a major protein) in the absence of other causes for such abnormalities. SCLS is thus a limb- and life-threatening illness, because each episode has the potential to cause damage to limb muscles and nerves, as well as to vital organs due to limited perfusion. It is often misdiagnosed as polycythemia, polycythemia vera, hyperviscosity syndrome, or sepsis.

Symptoms of high blood sugar including increased thirst (polydipsia), increased volume of urination (polyurea), and increase hunger (polyphagia).

Symptoms of HHS include:

- Altered level of consciousness

- Neurologic signs including: blurred vision, headaches, focal seizures, myoclonic jerking, reversible paralysis

- Motor abnormalities including flaccidity, depressed reflexes, tremors or fasiciculations

- Hyperviscosity and increased risk of blood clot formation

- Dehydration

- Weight loss

- Nausea, vomiting, and abdominal pain

- Weakness

- Low blood pressure with standing

The major differential diagnosis is diabetic ketoacidosis (DKA). In contrast to DKA, serum glucose levels in HHS are extremely high, usually greater than 40-50 mmol/L (600 mg/dL). Metabolic acidosis is absent or mild. A temporary state of confusion (delirium) is also more common in HHS than DKA. HHS also tends to affect older people more. DKA may have fruity breath, and rapid and deep breathing.

DKA often has serum glucose level greater than 300 mg/dL (HHS is >600 mg/dL). DKA usually occurs in type 1 diabetics whereas HHS is more common in type 2 diabetics. DKA is characterized by a rapid onset, and HHS occurs gradually over a few days. DKA also is characterized by ketosis due to the breakdown of fat for energy.

Both DKA and HHS may show symptoms of dehydration, increased thirst, increased urination, increased hunger, weight loss, nausea, vomiting, abdominal pain, blurred vision, headaches, weakness, and low blood pressure with standing.

The diagnosis is made by x-ray/MRI appearance and has five juxta-articular classifications and forehead, neck, and shaft classifications indicating early radiological signs.

Early on there is flattening of articular surfaces, thinning of cartilage with osteophyte (spur) formation. In juxta-articular lesions without symptoms, there is dead bone and marrow separated from living bone by a line of dense collagen. Microscopic cysts form, fill with necrotic material and there is massive necrosis with replacement by cancellous bone with collapse of the lesions.

The lesion begins as a random finding on x-ray without symptoms. Symptomatic lesions usually involve joint surfaces, and fracture with attempted healing occurs. This process takes place over months to years and eventually causes disabling arthritis, particularly of the femoral head (hip).

The following staging system is sometimes useful when managing lesions.

- Stage 0 - Intravascular coagulation

- Stage 1 - Dead Bone without repair

- Stage 2 - Dead Bone with repair but without collapse

- Stage 3 - Dead Bone with repair and with collapse

- Stage 4 - Secondary degenerative arthritis

In a study of bone lesions in 281 compressed air workers done by Walder in 1969, 29% of the lesions were in the humeral head (shoulder), 16% in the femoral head (hip), 40% in the lower end of the femur (lower thigh at the knee) and 15% in the upper tibia (knee below the knee cap).

Worsening of the condition from continued decompression in an asymptomatic x-ray finding may occur.

Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers. Although the definitive pathologic process is poorly understood, there are several hypotheses:

- Intra- or extravascular nitrogen in bones, "nitrogen embolism".

- Osmotic gas effects due to intramedullary pressure effects.

- fat embolism

- hemoconcentration and increased coagulability.

OHSS is divided into the categories mild, moderate, severe, and critical.

In mild forms of OHSS the ovaries are enlarged (5–12 cm) and there may be additional accumulation of ascites with mild abdominal distension, abdominal pain, nausea, and diarrhea. In severe forms of OHSS there may be hemoconcentration, thrombosis, distension, oliguria (decreased urine production), pleural effusion, and respiratory distress. Early OHSS develops before pregnancy testing and late OHSS is seen in early pregnancy.

Criteria for severe OHSS include enlarged ovary, ascites, hematocrit > 45%, WBC > 15,000, oliguria, creatinine 1.0-1.5 mg/dl, creatinine clearance > 50 ml/min, liver dysfunction, and anasarca. Critical OHSS includes enlarged ovary, tense ascites with hydrothorax and pericardial effusion, hematocrit > 55%, WBC > 25,000, oligoanuria, creatinine > 1.6 mg/dl, creatinine clearance < 50 ml/min, renal failure, thromboembolic phenomena, and ARDS.

Symptoms are set into 3 categories: mild, moderate, and severe. Mild symptoms include abdominal bloating and feeling of fullness, nausea, diarrhea, and slight weight gain. Moderate symptoms include excessive weight gain (weight gain of greater than 2 pounds per day), increased abdominal girth, vomiting, diarrhea, darker urine, decreased urine output, excessive thirst, and skin and/or hair feeling dry (in addition to mild symptoms). Severe symptoms are fullness/bloating above the waist, shortness of breath, pleural effusion, urination significantly darker or has ceased, calf and chest pains, marked abdominal bloating or distention, and lower abdominal pains (in addition to mild and moderate symptoms).

The characteristic symptoms of dengue are sudden-onset fever, headache (typically located behind the eyes), muscle and joint pains, and a rash. The alternative name for dengue, "breakbone fever", comes from the associated muscle and joint pains. The course of infection is divided into three phases: febrile, critical, and recovery.

The febrile phase involves high fever, potentially over , and is associated with generalized pain and a headache; this usually lasts two to seven days. Nausea and vomiting may also occur. A rash occurs in 50–80% of those with symptoms in the first or second day of symptoms as flushed skin, or later in the course of illness (days 4–7), as a measles-like rash. A rash described as "islands of white in a sea of red" has also been observed. Some petechiae (small red spots that do not disappear when the skin is pressed, which are caused by broken capillaries) can appear at this point, as may some mild bleeding from the mucous membranes of the mouth and nose. The fever itself is classically biphasic or saddleback in nature, breaking and then returning for one or two days.

In some people, the disease proceeds to a critical phase as fever resolves. During this period, there is leakage of plasma from the blood vessels, typically lasting one to two days. This may result in fluid accumulation in the chest and abdominal cavity as well as depletion of fluid from the circulation and decreased blood supply to vital organs. There may also be organ dysfunction and severe bleeding, typically from the gastrointestinal tract. Shock (dengue shock syndrome) and hemorrhage (dengue hemorrhagic fever) occur in less than 5% of all cases of dengue, however those who have previously been infected with other serotypes of dengue virus ("secondary infection") are at an increased risk. This critical phase, while rare, occurs relatively more commonly in children and young adults.

The recovery phase occurs next, with resorption of the leaked fluid into the bloodstream. This usually lasts two to three days. The improvement is often striking, and can be accompanied with severe itching and a slow heart rate. Another rash may occur with either a maculopapular or a vasculitic appearance, which is followed by peeling of the skin. During this stage, a fluid overload state may occur; if it affects the brain, it may cause a reduced level of consciousness or seizures. A feeling of fatigue may last for weeks in adults.

Dengue can occasionally affect several other body systems, either in isolation or along with the classic dengue symptoms. A decreased level of consciousness occurs in 0.5–6% of severe cases, which is attributable either to inflammation of the brain by the virus or indirectly as a result of impairment of vital organs, for example, the liver.

Other neurological disorders have been reported in the context of dengue, such as transverse myelitis and Guillain–Barré syndrome. Infection of the heart and acute liver failure are among the rarer complications.

A pregnant woman who develops dengue may be at a higher risk of miscarriage as well as low birth weight and premature birth.