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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)
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Pallor mortis (Latin: "pallor" "paleness", "mortis" "of death"), the first stage of death, is an after death paleness that occurs in those with light/white skin.
Pallor mortis occurs almost immediately (within 15–25 minutes) post-mortem; paleness develops so rapidly after death that it has little to no use in determining the time of death, aside from saying that it either happened less than 30 minutes ago or more, which could help if the body were found very soon after death.
There are numerous alternative remedies for motion sickness. One such is ginger, but it is ineffective.
Medications that may alleviate the symptoms of airsickness include:
- meclozine
- dimenhydrinate
- diphenhydramine
- scopolamine (available in both patch and oral form).
Pilots who are susceptible to airsickness should not take anti-motion sickness medications (prescription or over-the-counter). These medications can make one drowsy or affect brain functions in other ways.
The degree of rigor mortis may be used in forensic pathology, to determine the approximate time of death. A dead body holds its position as rigor mortis sets in. If the body is moved after death, but before rigor mortis begins, forensic techniques such as livor mortis can be applied. If the position in which a body is found does not match the location where it is found (for example, if it is flat on its back with one arm sticking straight up), that could mean someone moved it.
Several factors also affect the progression of rigor mortis, and investigators take these into account when estimating the time of death. One such factor is the ambient temperature. When conditions are warm, the onset and pace of rigor mortis are sped up by providing a conducive environment for the metabolic processes that cause decay. Low temperatures, however, slow them down. Therefore, for a person who dies outside in frozen conditions rigor mortis may last several days more than normal, so investigators may have to abandon it as a tool for determining time of death.
The clinician must protect the patient against hypotension, renal failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas.
Intravenous hydration of up to 1.5 L/hour should continue to prevent hypotension. A urinary output of at least 300 ml/hour should be maintained with IV fluids and mannitol, and hemodialysis considered if this amount of diuresis is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys.
To prevent hyperkalemia/hypocalcemia, consider the following adult doses:
- calcium gluconate 10% 10ml or calcium chloride 10% 5 ml IV over 2 minutes
- sodium bicarbonate 1 meq/kg IV slow push
- regular insulin 5–10 U
- 50% glucose 1–2 ampules IV bolus
- kayexalate 25–50 g with sorbitol 20% 100 ml by mouth or rectum.
Even so, cardiac arrhythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.
Fournier gangrene is a urological emergency requiring intravenous antibiotics and debridement (surgical removal) of necrotic (dead) tissue. In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) may be useful and acts to inhibit the growth of and kill the anaerobic bacteria.
Rigor mortis (Latin: "rigor" "stiffness", "mortis" "of death"), the third stage of death, is one of the recognizable signs of death, caused by chemical changes in the muscles post mortem, which cause the limbs of the corpse to stiffen. In humans, rigor mortis can occur as soon as 4 hours post mortem.
Putrefaction is the fifth stage of death, following pallor mortis, algor mortis, rigor mortis, and livor mortis. This process references the breaking down of a body of a human or animal post mortem (meaning after death). In broad terms, it can be viewed as the decomposition of proteins, and the eventual breakdown of the cohesiveness between tissues, and the liquefaction of most organs. This is caused by the decomposition of organic matter by bacterial or fungal digestion, which causes the release of gases that infiltrate the body's tissues, and leads to the deterioration of the tissues and organs.
The approximate time it takes putrefaction to occur is dependent on various factors. Internal factors that affect the rate of putrefaction include the age at which death has occurred, the overall structure and condition of the body, the cause of death, and external injuries arising before or after death. External factors include environmental temperature, moisture and air exposure, clothing, burial factors, and light exposure.
The first signs of putrefaction are signified by a greenish discoloration on the outside the skin on the abdominal wall corresponding to where the large intestine begins, as well as under the surface of the liver.
Certain substances, such as carbolic acid, arsenic, strychnine, and zinc chloride, can be used to delay the process of putrefaction in various ways based on their chemical make up. At body farms, facilities which study the process of decomposition as well as how these substances affect the rate of putrefaction, cadavers are put in different environmental conditions to study how the process of decomposition can be affected. There are six University Body Farm Research Facilities in the world, all located within the United States, which include the University of Tennessee at Knoxville, Western Carolina University, Texas State University, Sam Houston State University, Southern Illinois University, and Colorado Mesa University. Two prospective body farms will open outside the United States, in Australia and India.
The initial treatment of nicotine poisoning may include the administration of activated charcoal to try to reduce gastrointestinal absorption. Treatment is mainly supportive and further care can include control of seizures with the administration of a benzodiazepine, intravenous fluids for hypotension, and administration of atropine for bradycardia. Respiratory failure may necessitate respiratory support with rapid sequence induction and mechanical ventilation. Hemodialysis, hemoperfusion or other extracorporeal techniques do not remove nicotine from the blood and are therefore not useful in enhancing elimination. Acidifying the urine could theoretically enhance nicotine excretion, although this is not recommended as it may cause complications of metabolic acidosis.
Most patients experience an improvement of their symptoms, but for some, OI can be gravely disabling and can be progressive in nature, particularly if it is caused by an underlying condition which is deteriorating. The ways in which symptoms present themselves vary greatly from patient to patient; as a result, individualized treatment plans are necessary.
OI is treated both pharmacologically and non-pharmacologically. Treatment does not cure OI; rather, it controls symptoms.
Physicians who specialize in treating OI agree that the single most important treatment is drinking more than two liters (eight cups) of fluids each day. A steady, large supply of water or other fluids reduces most, and for some patients all, of the major symptoms of this condition. Typically, patients fare best when they drink a glass of water no less frequently than every two hours during the day, instead of drinking a large quantity of water at a single point in the day.
For most severe cases and some milder cases, a combination of medications are used. Individual responses to different medications vary widely, and a drug which dramatically improves one patient's symptoms may make another patient's symptoms much worse. Medications focus on three main issues:
Medications that increase blood volume:
- Fludrocortisone (Florinef)
- Erythropoietin
- Hormonal contraception
Medications that inhibit acetylcholinesterase:
- Pyridostigmine
Medications that improve vasoconstriction:
- Stimulants: (e.g., Ritalin or Dexedrine)
- Midodrine (ProAmatine)
- Ephedrine and pseudoephedrine (Sudafed)
- Theophylline (low-dose)
- Selective serotonin reuptake inhibitors (SSRI's - Prozac, Zoloft, and Paxil)
Behavioral changes that patients with OI can make are:
- Avoiding triggers such as prolonged sitting, quiet standing, warm environments, or vasodilating medications
- Using postural maneuvers and pressure garments
- Treating co-existing medical conditions
- Increasing fluid and salt intake
- Physical therapy and exercise unless contraindicated by an underlying condition such as chronic fatigue syndrome where traditional exercise can worsen the condition
Certain poisonous substances to the body can delay the process of putrefaction. They include:
- Carbolic acid (Phenol)
- Arsenic and antimony
- Strychnine
- Nux Vomica (Plant)
- Zinc chloride, ZnCl
If someone is stranded in a harness, but is not unconscious or injured, and has something to kick against or stand on (such as a rock ledge or caving leg-loops) it is helpful for them to use their leg muscles by pushing against it every so often, to keep the blood pumping back to the torso. If the person is stranded in mid-air or is exhausted, then keeping the legs moving can be both beneficial and rather dangerous. On the one hand, exercising the leg muscles will keep the blood returning to the torso, but on the other hand, as the movements become weaker the leg muscles will continue to demand blood yet they will become much less effective at returning it to the body, and the moment the victim ceases moving their legs, the blood will immediately start to pool. "Pedaling an imaginary bicycle" should only be used as a last-ditch effort to prolong consciousness, because as soon as the "pedaling" stops, fainting will shortly follow. If it is impossible to rescue someone immediately, then it is necessary to raise their legs to a sitting position, which can be done with a loop of rigging tape behind the knees or specialized equipment from a rescue kit.
When workers are suspended in their safety harnesses for long periods, they may suffer from blood pooling in the lower body. This can lead to suspension trauma. Once a worker is back on the ground after a fall has been arrested on a fall protection system, a worker should be placed in the “W” position. The “W” position is where a worker sits upright on the ground with their back/chest straight and their legs bent so that their knees are in line with the bottom of their chin. For added stability, make sure that the worker’s feet stay flat on the ground. In this position, a KED board can still be used if there are any potential spinal injuries and a worker needs stabilization before transport.
Once the worker is in this position, they will need to stay in that position for at least 30 minutes. Try to leave the worker in this position until their symptoms begin to subside. The time in the “W” position will allow the pooled blood from the legs to be slowly re-introduced back into the body. By slowing the rate at which the pooled blood reaches different organs, you are giving the body more of an opportunity to filter the pooled blood and maintain internal homeostasis. http://www.rigidlifelines.com/blog/entry/suspension-traumasymptoms-and-treatment
As mentioned, permissive hypotension is unwise. Especially if the crushing weight is on the patient more than 4 hours, but often if it persists more than one hour, careful fluid overload is wise, as well as the administration of intravenous sodium bicarbonate. The San Francisco emergency services protocol calls for a basic adult dose of a 2 L bolus of normal saline followed by 500 ml/h, limited for "pediatric patients and patients with history of cardiac or renal dysfunction."
If the patient cannot be fluid loaded, this may be an indication for a tourniquet to be applied.
Prevention of suspension trauma is preferable to dealing with its consequences. Specific recommendations for individuals doing technical ropework are to avoid exhausting themselves so much that they end up without the energy to keep moving, and making sure everyone in a group is trained in single rope rescue techniques, especially the "single rope pickoff", a rather difficult technical maneuver that must be practiced frequently for smooth performance.
Good nutrition with adequate intake of iron may prevent this disorder. Good nutrition should also include balanced diet and exercise.
Patients generally respond well to treatment. Iron supplementation usually resolves the anemia, and corrects the glossodynia (tongue pain).
No treatment is required and the patches in time will settle.
The redness, scale and itch if present may be managed with simple emollients and sometimes hydrocortisone, a weak steroid, is also used.
As the patches of pityriasis alba do not darken normally in sunlight, effective sun protection helps minimise the discrepancy in colouration against the surrounding normal skin. Cosmetic camouflage may be required.
Tacrolimus has been reported as speeding resolution.
In exceptionally severe cases PUVA therapy may be considered.
Another type of thrombolysis disrupts the clot mechanically using either saline jets or, more recently, ultrasound waves. Saline jets dislodge the clot using the Bernoulli effect. Ultrasound waves, emitted at low frequency, create a physical fragmentation of the thrombus.
Exercise can improve symptoms, as can revascularization. Both together may be better than one intervention of its own.
Pharmacological options exist, as well. Medicines that control lipid profile, diabetes, and hypertension may increase blood flow to the affected muscles and allow for increased activity levels. Angiotensin converting enzyme inhibitors, beta-blockers, antiplatelet agents (aspirin and clopidogrel), naftidrofuryl, pentoxifylline, and cilostazol (selective PDE3 inhibitor) are used for the treatment of intermittent claudication. However, medications will not remove the blockages from the body. Instead, they simply improve blood flow to the affected area.
Catheter-based intervention is also an option. Atherectomy, stenting, and angioplasty to remove or push aside the arterial blockages are the most common procedures for catheter-based intervention. These procedures can be performed by interventional radiologists, interventional cardiologists, vascular surgeons, and thoracic surgeons, among others.
Surgery is the last resort; vascular surgeons can perform either endarterectomies on arterial blockages or perform an arterial bypass. However, open surgery poses a host of risks not present with catheter-based interventions.
Those unsuitable for surgery may receive thrombolytics. In the past, streptokinase was the main thrombolytic chemical. More recently, drugs such as tissue plasminogen activator, urokinase, and anisterplase have been used in its place. Mechanical methods of injecting the thrombolytic compounds have improved with the introduction of pulsed spray catheters—which allow for a greater opportunity for patients to avoid surgery. Pharmacological thrombolysis requires a catheter insert into the affected area, attached to the catheter is often a wire with holes to allow for a wider dispersal area of the thrombolytic agent. These agents lyse the ischemia-causing thrombus quickly and effectively. However, the efficacy of thrombolytic treatment is limited by hemorrhagic complications. Plasma fibrinogen level has been proposed as a predictor of these hemorrhagic complications. However, based on a systemtic review of the available literature until January 2016, the predictive value of plasma is unproven.
The goal of treatment is to reduce inflammation. Treatment usually does not require hospitalization unless tongue swelling is severe. Good oral hygiene is necessary, including thorough tooth brushing at least twice a day, and flossing at least daily. Corticosteroids such as prednisone may be given to reduce the inflammation of glossitis. For mild cases, topical applications (such as a prednisone mouth rinse that is not swallowed) may be recommended to avoid the side effects of swallowed or injected corticosteroids. Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of glossitis is an infection. Anemia and nutritional deficiencies (such as a deficiency in niacin, riboflavin, iron, or Vitamin E) must be treated, often by dietary changes or other supplements. Avoid irritants (such as hot or spicy foods, alcohol, and tobacco) to minimize the discomfort.
In some cases, tongue swelling may threaten the airway, a medical emergency that needs immediate attention.
Blood transfusion is sometimes used to treat iron deficiency with hemodynamic instability. Sometimes transfusions are considered for people who have chronic iron deficiency or who will soon go to surgery, but even if such people have low hemoglobin, they should be given oral treatment or intravenous iron.
Before commencing treatment, there should be definitive diagnosis of the underlying cause for iron deficiency. This is particularly the case in older patients, who are most susceptible to colorectal cancer and the gastrointestinal bleeding it often causes. In adults, 60% of patients with iron deficiency anemia may have underlying gastrointestinal disorders leading to chronic blood loss.
It is likely that the cause of the iron deficiency will need treatment as well.
Upon diagnosis, the condition can be treated with iron supplements. The choice of supplement will depend upon both the severity of the condition, the required speed of improvement (e.g. if awaiting elective surgery) and the likelihood of treatment being effective (e.g. if has underlying IBD, is undergoing dialysis, or is having ESA therapy).
Examples of oral iron that are often used are ferrous sulfate, ferrous gluconate, or amino acid chelate tablets. Recent research suggests the replacement dose of iron, at least in the elderly with iron deficiency, may be as little as 15 mg per day of elemental iron.
Early treatment is essential to keep the affected limb viable. The treatment options include injection of an anticoagulant, thrombolysis, embolectomy, surgical revascularisation, or amputation. Anticoagulant therapy is initiated to prevent further enlargement of the thrombus. Continuous IV unfractionated heparin has been the traditional agent of choice.
If the condition of the ischemic limb is stabilized with anticoagulation, recently formed emboli may be treated with catheter-directed thrombolysis using intraarterial infusion of a thrombolytic agent (e.g., recombinant tissue plasminogen activator (tPA), streptokinase, or urokinase). A percutaneous catheter inserted into the femoral artery and threaded to the site of the clot is used to infuse the drug. Unlike anticoagulants, thrombolytic agents work directly to resolve the clot over a period of 24 to 48 hours.
Direct arteriotomy may be necessary to remove the clot. Surgical revascularization may be used in the setting of trauma (e.g., laceration of the artery). Amputation is reserved for cases where limb salvage is not possible. If the patient continues to have a risk of further embolization from some persistent source, such as chronic atrial fibrillation, treatment includes long-term oral anticoagulation to prevent further acute arterial ischemic episodes.
Decrease in body temperature reduces the aerobic metabolic rate of the affected cells, reducing the immediate effects of hypoxia. Reduction of body temperature also reduces the inflammation response and reperfusion injury. For frostbite injuries, limiting thawing and warming of tissues until warmer temperatures can be sustained may reduce reperfusion injury.