Disseminated coagulation:

also known as disseminated intravascular coagulopathy or less commonly as consumptive coagulopathy, is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleedingoccurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result.

Disseminated coagulation:

Infections: Gram-negative sepsis, Neisseria meningitidis, Streptococcus pneumoniae, malaria, histoplasmosis, aspergillosis, Rocky mountain spotted fever Miscellaneous: Liver disease, snake bite, giant hemangioma, shock, heat stroke, vasculitis, aortic aneurysm, Serotonin syndrome[8] Viral: Arenaviruses causing Argentine hemorrhagic fever or Bolivian Hemorrhagic Fever

Causes:
DIC can occur in the following conditions: Cancers of lung, pancreas, prostate and stomach, as well as acute myeloid leukemia (particularly APL) Obstetric: abruptio placentae, preeclampsia, amniotic fluid embolism, retained intrauterine fetal demise Massive tissue injury: Trauma, burns, extensive surgery

The affected person is often acutely ill and shocked with widespread hemorrhage (common bleeding sites are mouth, nose and venipuncture sites), extensive bruising, renal failure and gangrene.The onset of DIC can be fulminant, as in endotoxic shock or amniotic fluid embolism, or it may be insidious and chronic, as in cases of carcinomatosis.

Treatment:

The only effective treatment is the reversal of the underlying cause. Anticoagulants are given exceedingly rarely, only when thrombus formation is likely to lead to imminent death (such as in coronary artery thrombosis or cerebrovascular thrombosis).

Platelets may be transfused if counts are less than 5,000-10,000/mm3 and massive hemorrhage is occurring, and fresh frozen plasma may be administered in an attempt to replenish coagulation factors and antithrombotic factors, although these are only temporizing measures and may result in the increased development of thrombosis.

DIC results in lower fibrinogen levels (as it has all been converted to fibrin), and this can be tested for in the hospital lab. A more specific test is for "fibrin split products" (FSPs) or "fibrin degradation products" (FDPs) which are produced when fibrin undergoes degradation when blood clots are dissolved by fibrinolysis.In some situations, infusion with antithrombin may be necessary.

Perineal hematoma:

is a type of hematoma located in, or on the border of the anus.It is sometimes inappropriately referred to as an external hemorrhoid. A perianal hematoma is a collection of shape under the skin at the advantages of the rectal developing. Perianal hematoma is due to a distressing split of a small flow in this region due to large requirements due to driving. Many persons with a perianal hematoma can acceptance coaching something big, going house, having totes or youngsters, serious cough problem or driving with colon issues swiftly before they view that there is something wrong in their rectal region. Also, perianal hematoma is usually seen in persons performing out at health club, weight lifting, etc.

Signs and symptoms:

A perianal hematoma, identified by the typical blue tinge under the skin (to the left in the above image) The symptoms of a perianal hematoma can present over a short period of time. Pain, varying from mild to severe, will occur as the skin surrounding the rupture expands due to pressure. This pain will usually last even after the blood has clotted, and may continue for two to four days.

Causes:

Perianal hematoma are caused by the rupture of a small vein that drains blood from the anus.This rupture may be the result of forceful or strained bowel movement or caused by heavy lifting, coughing or straining. Once the rupture has formed, blood quickly pools within a few hours and, if left untreated, forms a clot.

Management:

If diagnosed within the first few hours of presentation, the pooling blood may be evacuated using a syringe. Once the blood has clotted, removal by this method is no longer possible and the clot can be removed via an incision over the lump under local anesthetic. The incision is not stitched, but will heal very well. Care needs to be taken in regard to bleeding from the wound and possible infection with fecal bacteria. If left alone it will usually heal within a few days or weeks

Urinary retention:

is a lack of ability to urinate. It is a common complication of benign prostatic hyperplasia (BPH), although it can also be caused by nerve dysfunction, constipation, infection, or medications (including anticholinergics, antidepressants, COX-2 inhibitors,amphetamines and opiates). Diagnosis and/or treatment may require use of a catheter or prostatic stent.

Signs and symptoms:

Urinary retention is characterised by poor urinary stream with intermittent flow, straining, a sense of incomplete voiding and hesitancy (a delay between trying to urinate and the flow actually beginning). As the bladder remains full, it may lead to incontinence, nocturia (need to urinate at night) and high frequency. Acute retention causing complete anuria is a medical emergency, as the bladder may distend (stretch) to enormous sizes and possibly tear if not dealt with quickly.

If the bladder distends enough it will begin to become painful. The increase in pressure in the bladder can also prevent urine from entering the ureters or even cause urine to pass back up the ureters and get into the kidneys, causing hydronephrosis, and possibly pyonephrosis, kidney failure and sepsis. A person should go straight to an emergency department or A&E service as soon as possible if unable to urinate when having a painfully full bladder.

Causes:
->In the bladder: Detrusor sphincter dyssynergia Neurogenic bladder (commonly pelvic splanchic nerve damage, cauda equina syndrome, descending cortical fibers lesion, pontine micturation or storage center lesions, demyelinating diseases or Parkinson's disease) Iatrogenic (caused by medical treatment/procedure) scarring of the bladder neck (commonly from removal of indwelling catheters or cystoscopy operations)

->In the prostate Benign prostatic hyperplasia Prostate cancer and other pelvic malignancies Prostatitis

->Penile urethra Congenital urethral valves Phimosis or pinhole meatus Circumcision Obstruction in the urethra, for example a metastasis or a precipitated pseudogout crystal in the urine STD lesions (gonorrhoea causes numerous strictures, leading to a "rosary bead" appearance, whereas chlamydia usually causes a single stricture)

Treatment:

In acute urinary retention, urinary catheterization, placement of a prostatic stent or suprapubic cystostomy relieves the retention. In the longer term, treatment depends on the cause. BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral resection of the prostate (TURP). Older patients with ongoing problems may require continued intermittent self catheterization.5-alpha-reductase inhibitor increase the chance of normal urination following catheter removal.

Pulmonary Embolus:

is a blockage of the main artery of the lung or one of its branches by a substance that has traveled from elsewhere in the body through the bloodstream (embolism). PE most commonly results from deep vein thrombosis (a blood clot in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, a process termed venous thromboembolism (VTE).

A small proportion of cases are due to the embolization of air, fat, talc in drugs of intravenous drug abusers or amniotic fluid. The obstruction of the blood flow through the lungs and the resultant pressure on the right ventricle of the heart lead to the symptoms and signs of PE. The risk of PE is increased in various situations, such as cancer or prolonged bed rest.

Signs and symptoms:

Symptoms of PE are typically sudden in onset and include dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability due to decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE.

On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is transudative, detectable by decreased percussion note, audible breath sounds and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and raised jugular venous pressure.A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.

Diagnosis:

To diagnose pulmonary embolism, medical societies recommend a review of clinical criteria to determine the need for testing, followed by testing to determine a likelihood of being able to confirm a diagnosis by imaging, followed by imaging if other tests have shown that there is a likelihood of a PE diagnosis.

The diagnosis of PE is based primarily on validated clinical criteria combined with selective testing because the typical clinical presentation (shortness of breath, chest pain) cannot be definitively differentiated from other causes of chest pain and shortness of breath. The decision to do medical imaging is usually based on clinical grounds, i.e. the medical history, symptoms and findings on physical examination, followed by an assessment of clinical probability

Subinvolution:

is a medical condition in which after childbirth, the uterus does not return to its normal size. When the involution is impaired or retarded it is called subinvolution. The uterus is the most common organ affected by subinvolution. As it is the most accessible organ to be measured per abdomen, the uterine involution is considered clinically as an index to assess subinvolution.

Signs and Symptoms:

The uterine height is greater than the normal for the particular day of puerperium. Normal puerperal uterus may be displaced by a full bladder or a loaded rectum. It feels boggy and softer upon palpation. Abnormal lochial discharge either excessive or prolonged Irregular or at times excessive uterine bleeding Irregular cramp like pain is cases of retained products or rise of temperature in sepsis

Factors:

Persistent lochia/fresh bleeding Long labor anaesthesia full bladder difficult delivery retained placenta maternal infection

Causes:

->Predisposing factors grand multiparity overdistension of uterus as in twins and hydramnios ill maternal health caesarean section uterine prolapse retroversion after the uterus becomes pelvic organ uterine fibroid

Management:

Antibiotics in endometritis Exploration of the uterus in retained products Ergometrine so often prescribed to enhance the involution process by reducing the blood flow of the uterus is of no value in prophylaxis.