Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
The eyes may show retinal hemorrhage or an exudate. Papilledema must be present before a diagnosis of malignant hypertension can be made. The brain shows manifestations of increased intracranial pressure, such as headache, vomiting, and/or subarachnoid or cerebral hemorrhage. Patients will usually suffer from left ventricular dysfunction. The kidneys will be affected, resulting in hematuria, proteinuria, and acute renal failure. It differs from other complications of hypertension in that it is accompanied by papilledema. This can be associated with hypertensive retinopathy.
Other signs and symptoms can include:
- Chest pain
- Arrhythmias
- Headache
- Epistaxis
- Dyspnea
- Faintness or vertigo
- Severe anxiety
- Agitation
- Altered mental status
- Paresthesias
- Vomiting
Chest pain requires immediate lowering of blood pressure (such as with sodium nitroprusside infusions), while urgencies can be treated with oral agents, with the goal of lowering the mean arterial pressure (MAP) by 20% in 1–2 days with further reduction to "normal" levels in weeks or months. The former use of oral nifedipine, a calcium channel blocker, has been strongly discouraged as it has led to excessive falls in blood pressure with serious and fatal consequences.
Sometimes, the term hypertensive emergency is also used as a generic term, comprising both hypertensive "emergency", as a specific term for a serious and urgent condition of elevated blood pressure, and hypertensive urgency, as a specific term of a less serious and less urgent condition (the terminology hypertensive "crisis" is usually used in this sense).
Severely elevated blood pressure (equal to or greater than a systolic 180 or diastolic of 110—sometimes termed malignant or accelerated hypertension) is referred to as a "hypertensive crisis", as blood pressure at this level confers a high risk of complications. People with blood pressures in this range may have no symptoms, but are more likely to report headaches (22% of cases) and dizziness than the general population. Other symptoms accompanying a hypertensive crisis may include visual deterioration due to retinopathy, breathlessness due to heart failure, or a general feeling of malaise due to kidney failure. Most people with a hypertensive crisis are known to have elevated blood pressure, but additional triggers may have led to a sudden rise.
A "hypertensive emergency" is diagnosed when there is evidence of direct damage to one or more organs as a result of severely elevated blood pressure greater than 180 systolic or 120 diastolic. This may include hypertensive encephalopathy, caused by brain swelling and dysfunction, and characterized by headaches and an altered level of consciousness (confusion or drowsiness). Retinal papilledema and/or fundal bleeds and exudates are another sign of target organ damage. Chest pain may indicate heart muscle damage (which may progress to myocardial infarction) or sometimes aortic dissection, the tearing of the inner wall of the aorta. Breathlessness, cough, and the coughing up of blood-stained sputum are characteristic signs of pulmonary edema, the swelling of lung tissue due to left ventricular failure an inability of the left ventricle of the heart to adequately pump blood from the lungs into the arterial system. Rapid deterioration of kidney function (acute kidney injury) and microangiopathic hemolytic anemia (destruction of blood cells) may also occur. In these situations, rapid reduction of the blood pressure is mandated to stop ongoing organ damage. In contrast there is no evidence that blood pressure needs to be lowered rapidly in hypertensive urgencies where there is no evidence of target organ damage and over aggressive reduction of blood pressure is not without risks. Use of oral medications to lower the BP gradually over 24 to 48h is advocated in hypertensive urgencies.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120 mmHg or systolic blood pressure greater than or equal to 180 mmHg. Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
Distributive shock is a medical condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body's tissues and organs. It is one of four categories of shock, a condition where there is not enough oxygen-carrying blood to meet the metabolic needs of the cells which make up the body's tissues and organs. Distributive shock is different from the other three categories of shock in that it occurs even though the output of the heart is at or above a normal level. The most common cause is sepsis leading to type of distributive shock called septic shock, a condition that can be fatal.
Waterhouse-Friderichsen Syndrome can be caused by a number of different organisms (see below). When caused by Neisseria meningitidis, WFS is considered the most severe form of meningococcal sepsis. The onset of the illness is nonspecific with fever, rigors, vomiting, and headache. Soon a rash appears; first macular, not much different from the rose spots of typhoid, and rapidly becoming petechial and purpuric with a dusky gray color. Low blood pressure (hypotension) develops and rapidly leads to septic shock. The cyanosis of extremities can be extreme and the patient is very prostrated or comatose. In this form of meningococcal disease, meningitis generally does not occur. Low levels of blood glucose and sodium, high levels of potassium in the blood, and the ACTH stimulation test demonstrate the acute adrenal failure. Leukocytosis need not be extreme and in fact leukopenia may be seen and it is a very poor prognostic sign. C-reactive protein levels can be elevated or almost normal. Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features.
Hypovolemia is a direct loss of effective circulating blood volume leading to:
- A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia
- Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
- Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis
- Hypothermia due to decreased perfusion and evaporation of sweat
- Thirst and dry mouth, due to fluid depletion
- Cold and mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin
The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. This approximates to the effective loss of blood volume. The "shock index" (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone. This relationship has not been well established in pregnancy-related bleeding.
In addition to sepsis, distributive shock can be caused by systemic inflammatory response syndrome (SIRS) due to conditions other than infection such as pancreatitis, burns or trauma. Other causes include, toxic shock syndrome (TSS), anaphylaxis (a sudden, severe allergic reaction), adrenal insufficiency, reactions to drugs or toxins, heavy metal poisoning, hepatic (liver) insufficiency and damage to the central nervous system. Causes of adrenal insufficiency leading to distributive shock include acute worsening of chronic adrenal insufficiency, destruction or removal of the adrenal glands, suppression of adrenal gland function due to exogenous steroids, hypopituitarism and metabolic failure of hormone production.
The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness. While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present. While a fast heart rate is common, those on β-blockers, those who are athletic and in 30% of cases of those with shock due to intra abdominal bleeding may have a normal or slow heart rate. Specific subtypes of shock may have additional symptoms.
Waterhouse–Friderichsen syndrome (WFS) is defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically it is caused by "Neisseria meningitidis".
The bacterial infection leads to massive bleeding into one or (usually) both adrenal glands. It is characterized by overwhelming bacterial infection meningococcemia leading to massive blood invasion, organ failure, coma, low blood pressure and shock, disseminated intravascular coagulation (DIC) with widespread purpura, rapidly developing adrenocortical insufficiency and death.
Characteristic symptoms are:
- Sudden penetrating pain in the legs, lower back or abdomen
- Confusion, psychosis, slurred speech
- Severe lethargy
- Convulsions
- Fever
- Hyperkalemia (elevated potassium level in the blood)
- Hypercalcemia (elevated calcium level in the blood): the cause of hypercalcemia is a combination of increased calcium input into the extracellular space and reduced calcium removal by the kidney, this last caused by decreased glomerular filtration and increased tubular calcium reabsorption. Both renal factors are secondary to volume depletion and, in fact, improve rapidly during rehydration with saline infusion.
- Hypoglycemia (reduced level of blood glucose)
- Hyponatremia (low sodium level in the blood)
- Hypotension (low blood pressure)
- Hypothyroid (low T4 level)
- Severe vomiting and diarrhea, resulting in dehydration
- Syncope (loss of consciousness and ability to stand)
Adrenal crisis (also known as Addisonian crisis and acute adrenal insufficiency) is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment. It is a constellation of symptoms that indicate severe adrenal insufficiency caused by insufficient levels of the hormone cortisol. This may be the result of either previously undiagnosed or untreated Addison's disease, a disease process suddenly affecting adrenal function (such as bleeding from the adrenal glands in Waterhouse-Friderichsen syndrome), suddenly stopping intake of glucocorticoids or an intercurrent problem (e.g. infection, trauma, in fact any form of physical or mental stress) in someone known to have Addison's disease or congenital adrenal hyperplasia (CAH).
The initial symptoms of pituitary apoplexy are related to the increased pressure in and around the pituitary gland. The most common symptom, in over 95% of cases, is a sudden-onset headache located behind the eyes or around the temples. It is often associated with nausea and vomiting. Occasionally, the presence of blood leads to irritation of the lining of the brain, which may cause neck rigidity and intolerance to bright light, as well as a decreased level of consciousness. This occurs in 24% of cases.
Pressure on the part of the optic nerve known as the chiasm, which is located above the gland, leads to loss of vision on the outer side of the visual field on both sides, as this corresponds to areas on the retinas supplied by these parts of the optic nerve; it is encountered in 75% of cases. Visual acuity is reduced in half, and over 60% have a visual field defect. The visual loss depends on which part of the nerve is affected. If the part of the nerve between the eye and the chiasm is compressed, the result is vision loss in one eye. If the part after the chiasm is affected, visual loss on one side of the visual field occurs.
Adjacent to the pituitary lies a part of the skull base known as the cavernous sinus. This contains a number of nerves that control the eye muscles. 70% of people with pituitary apoplexy experience double vision due to compression of one of the nerves. In half of these cases, the oculomotor nerve (the third cranial nerve), which controls a number of eye muscles, is affected. This leads to diagonal double vision and a dilated pupil. The fourth (trochlear) and sixth (abducens) cranial nerves are located in the same compartment and can cause diagonal or horizontal double vision, respectively. The oculomotor nerve is predominantly affected as it lies closest to the pituitary. The cavernous sinus also contains the carotid artery, which supplies blood to the brain; occasionally, compression of the artery can lead to one-sided weakness and other symptoms of stroke.
An acute abdomen refers to a sudden, severe abdominal pain. It is in many cases a medical emergency, requiring urgent and specific diagnosis. Several causes need surgical treatment.
Pituitary apoplexy or pituitary tumor apoplexy is bleeding into or impaired blood supply of the pituitary gland at the base of the brain. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously. The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland. This is followed in many cases by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency.
The diagnosis is achieved with magnetic resonance imaging and blood tests. Treatment is by the timely correction of hormone deficiencies, and in many cases surgical decompression is required. Many people who have had a pituitary apoplexy develop pituitary hormone deficiencies and require long-term hormone supplementation. The first case of the disease was recorded in 1898.
Individuals with TEC have a median age of presentation of 18–26 months; however, the disorder may occur in infants younger than 6 months and in children as old as age 10 years.
Because of the gradual onset of the anemia, children are often healthier than expected from their low hemoglobin levels.
Most patients recover completely within 1–2 months.
However many reported cases have lasted 18–24 months and longer.
The crisis is a common complication in sickle-cell patients and can be associated with one or more symptoms including fever, cough, excruciating pain, sputum production, shortness of breath, or low oxygen levels.
Acute chest syndrome is often precipitated by a lung infection, and the resulting inflammation and loss of oxygen saturation leads to further sickling of red cells, thus exacerbating pulmonary and systemic hypoxemia, sickling, and vaso-occlusion.
If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.
Most affected cats present with muscular weakness and/or ocular signs of hypertension. Signs of muscle weakness can include a plantigrade stance of the hindlimbs, cervical ventroflexion, inability to jump, lateral recumbency, or collapse. Ocular signs of arterial hypertension include mydriasis, hyphema, or blindness due to retinal detachment and/or intraocular hemorrhages. A palpable mass in the cranial abdomen is another potential finding.
The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.
Symptoms of hypoadrenocorticism can include vomiting, diarrhea, lethargy, lack of appetite, tremors or shaking, muscle weakness, low body temperature, collapse, low heart rate, and pain in the hind quarters. Hypoglycemia can also be present, and initially may be confused with seizure disorders, insulin-secreting pancreatic tumor (insulinoma), food poisoning, parvovirus enteritis, gastric volvulus, spinal or joint problems, earning hypoadrenocorticism the nicknames of "the Great Mimic" and "the Great Imitator". It is possible not to see any signs of the disease until 90% of the adrenal cortex is no longer functioning.
Patients with GRA may be asymptomatic, but the following symptoms can be present:
- Fatigue
- Headache
- High blood pressure
- Hypokalemia
- Intermittent or temporary paralysis
- Muscle spasms
- Muscle weakness
- Numbness
- Polyuria
- Polydipsia
- Tingling
- Hypernatraemia
- Metabolic alkalosis
Acute abdomen is occasionally used synonymously with peritonitis. While this is not entirely incorrect, peritonitis is the more specific term, referring to inflammation of the peritoneum. It manifests on physical examination as rebound tenderness, or pain upon "removal" of pressure more than on "application" of pressure to the abdomen. Peritonitis may result from several of the above diseases, notably appendicitis and pancreatitis. While rebound tenderness is commonly associated with peritonitis, the most specific finding is rigidity.
Arterial occlusion may be due to thrombi, amniotic fragments or air embolism. Postpartum cerebral angiopathy is a transitory arterial spasm of medium caliber cerebral arteries; it was first described in cocaine and amphetamine addicts, but can also complicate ergot and bromocriptine prescribed to inhibit lactation. Subarachnoid haemorrhage can occur after miscarriage or childbirth. Epidural anaesthesia can, if the dura is punctured, lead to leakage of Cerebrospinal fluid and subdural haematoma. All these can occasionally present with psychiatric symptoms.
Pituitary necrosis following postpartum haemorrhage (Sheehan’s syndrome) leads to failure and atrophy of the gonads, adrenal and thyroid. Chronic psychoses can supervene many years later, based on myxoedema, hypoglycaemia or Addisonian crisis. But these patients can also develop acute and recurrent psychoses, even as early as the puerperium.