Vasovagal (situational) syncope—one of the most common types—may occur in scary, embarrassing or uneasy situations, or during blood drawing, coughing, urination or defecation. Other types include postural syncope (caused by a changing in body posture), cardiac syncope (due to heart-related conditions), and neurological syncope (due to neurological conditions). There are many other causes of syncope, including low blood-sugar levels and lung disease such as emphysema and a pulmonary embolus. The cause of the fainting can be determined by a doctor using a complete history, physical, and various diagnostic tests.
The vasovagal type can be considered in two forms:
* Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group, and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
* Recurrent syncope with complex associated symptoms. This is so-called Neurally Mediated Syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, light-headedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive.
Cardiac arrhythmias is the most common cause of cardiac syncope. Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which requires DC cardioversion.
Aortic stenosis and mitral stenosis are the most common examples.Aortic stenosis presents with repeated episodes of syncope. Pulmonary embolism can cause obstructed blood vessels. High blood pressure in the arteries supplying the lungs (pulmonary artery hypertension) can occur during pulmonary embolism. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.
Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm).If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large.
The vast majority of aneurysms are asymptomatic. However, as abdominal aortic aneurysms expand, they may become painful and lead to pulsating sensations in the abdomen or pain in the chest, lower back, or scrotum.The risk of rupture is high in a symptomatic aneurysm, which is therefore considered an indication for surgery.The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.
The clinical manifestation of ruptured AAA usually includes excruciating pain of the lower back, flank, abdomen and groin. The bleeding usually leads to a hypovolemic shock with hypotension, tachycardia, cyanosis, and altered mental status. The mortality of AAA rupture is up to 90%. 65–75% of patients die before they arrive at hospital and up to 90% die before they reach the operating room.The bleeding can be retroperitoneal or intraperitoneal, or the rupture can create an aortocaval or aortointestinal (between the aorta and intestine) fistula.Flank ecchymosis is a sign of retroperitoneal hemorrhage, and is also called Grey Turner's sign.
The main sites of copper accumulation are the liver and the brain, and consequently liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis.
Liver disease may present as tiredness, increased bleeding tendency or confusion (due to hepatic encephalopathy) and portal hypertension. The latter, a condition in which the pressure in the portal vein is markedly increased, leads to esophageal varices that may bleed in a life-threatening fashion, splenomegaly and ascites. On examination, signs of chronic liver disease such as spider naevi may be observed. Chronic active hepatitis has caused cirrhosis of the liver in most by the time they develop symptoms. While most people with cirrhosis have an increased risk of hepatocellular carcinoma , this risk is relatively very low in Wilson's disease.
Various medical conditions have been linked with copper accumulation in Wilson's disease:
* Eyes: Kayser–Fleischer rings (KF rings) may be visible around the iris. They are due to copper deposition in Descemet's membrane of the cornea. They do not occur in all people and may only be visible on slit lamp examination.
Kidneys: renal tubular acidosis, a disorder of bicarbonate handling by the proximal tubules leads to nephrocalcinosis
About half the people with Wilson's have neurological or psychiatric problems.neurological symptoms then follow, often in the form of parkinsonism with or without a typical hand tremor, masked facial expressions, slurred speech, ataxia or dystonia . Seizures and migraine appear to be more common in Wilson's disease.
There is no totally reliable test for Wilson's disease, but levels of ceruloplasmin and copper in the blood, as well of the amount of copper excreted in urine during a 24-hour period, are together used to form an impression of the amount of copper in the body. The gold standard or most ideal test is a liver biopsy.
Generally, penicillamine is the first treatment used. This binds copper and leads to excretion of copper in the urine.Liver transplantation is an effective cure for Wilson's disease, but is used only in particular scenarios because of the numerous risks and complications associated with the procedure. It is used mainly in people with fulminant liver failure who fail to respond to medical treatment, or in those with advanced chronic liver disease.
* Delayed union
* Joint stiffness
* Myositis ossificans
* Avascular necrosis
* Algodystrophy (or Sudeck's atrophy)
* Growth disturbance or deformity
* Gangrene, tetanus, septicaemia
* Fear of mobilising
Nonunion is where there are no signs of healing after >3-6 months (depending upon the site of fracture). Nonunion is one endpoint of delayed union. Malunion occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction.
Causes of delayed union include:
* Severe soft tissue damage
* Inadequate blood supply
* Insufficient splintage
* Excessive traction
Nonunion occurs in approximately 1% of all fractures but is more common in lower leg fractures (19% nonunion) or where there is motion at the fracture site.
Nonsurgical approaches such as early weight bearing and casting may be helpful for delayed union and nonunion.
Surgical treatments include:
* Debridement to establish a healthy infection-free vascularity at the fracture site
* Internal fixation to reduce and stabilise the fracture.
* Bone grafting to stimulate new callus formation.
Certain regions are known for their propensity to develop ischemia and necrosis after injury.
It’s Early complication because ischemia occurs during the first few hours but the clinical and radiological effects are seen until weeks or months later . Avascular necrosis causes deformation of the bone. This leads, a few years later, to secondary osteoarthritis and causes painful limitation of joint movement.
An ECMO machine is similar to a heart-lung machine. To initiate ECMO, cannulae are placed in large blood vessels to provide access to the patient's blood. Anticoagulant drugs, usually heparin, are given to prevent blood clotting. The ECMO machine continuously pumps blood from the patient through a membrane oxygenator that imitates the gas exchange process of the lungs, i.e. it removes carbon dioxide and adds oxygen. Oxygenated blood is then returned to the patient. Management of the ECMO circuit is done by a team of ECMO specialists that includes intensive care unit (ICU) physicians, physician assistants, perfusionists, Registered Nurses, respiratory therapists, and Medical Laboratory Technologists that have received training in this specialty.
There are several forms of ECMO, the two most common of which are veno-arterial (VA) and veno-venous (VV). In both modalities, blood drained from the venous system is oxygenated outside of the body. In VA ECMO, this blood is returned to the arterial system and in VV ECMO the blood is returned to the venous system. In VV ECMO, no cardiac support is provided.
VV ECMO can provide sufficient oxygenation for several weeks, allowing diseased lungs to heal while the potential additional injury of aggressive mechanical ventilation is avoided. It may therefore be life-saving for some patients.
Fatal sepsis may occur when the large catheters inserted in the neck provide fertile field for infection.Additional risks include bleeding. In adults, ECMO survival rates are around 60%. ECMO has yet to have proven survival benefit in adults with acute respiratory distress syndrome (ARDS).
They do not always reflect liver diseases.
They may be a marker of worse health outcomes.
Isolated elevation of transaminases:
Medications (NSAIDs, Anitbiotics, statins,
antiepileptics and herbal preparations)
Alcohol (AST/ALT >2:1, twofold elevation
Hereditary hemochromatosis (Caucasian, iron,
TIBC, ferritin +/- liver biospy)
Viral hepatitis: HBV ( HBsAg, anti HBsAg, anti HBc) and HCV ( ELISA, RIBA, PCR )
Hepatic steatosis and NASH ( AST/ALT<1, ultrasound, CT or MRI)
Muscular disorders (AST/ALT>3 if immediately after injury, CK, LDH, aldoalse)
Thyroid diseases (TSH)
Celiac disease (ALT>AST, reversible with gluten free diet)
Adrenal insufficency ( reversible within week of treatment)
Wilson ‘s disease (age 5-25, serum ceruloplasmin, 24hr urine for copper, liver biopsy)
Autoimmune hepatitis ( SPEP, ANA , SMA, LKMA, liver biopsy)
Alpha 1 antitrypsin (associated emphysema, protein electrophoresis)
Hemolysis (smear, retic count, haptoglobin) can be inherited or acquired. Rarely exceeds 5mg/dl
Impaired uptake or conjugation, drugs, Crigller Najjar and Gilbert’s syndrome.
Dubin Johnson with altered excretion
Rotor syndrome with defective storage.
Isolated elevation of alkaline phosphatase
Alkaline phosphatase is derived from liver, bones, intestins and placenta.
Levels vary with age, more elevated in children.
To determine the source we check GGT or 5’ nucleotidase.
Initial evaluation includes U/S and AMA followed by ERCP v/s liver biopsy.
Isolated elevation of GGT
Very sensisitive for hepatobiliary disease but not specific.
Can reflect pancreatic disease, MI, renal failure, diabetes, COPD, alcoholism.
Histologically a wire-loop lesion will be present. The wire loop lesion is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop.
Furthermore, patients may suffer from other symptoms of lupus unrelated to kidney function. Such symptoms can include arthritis, fevers, gastro-intestinal disturbances, headaches, fatigue, and fluid in the joints.
The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy.
The World Health Organization has divided lupus nephritis into five classes based on the biopsy.
* Class I is minimal mesangial glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits on electron microscopy.
* Class II is based on a finding of mesangial proliferative lupus nephritis. This form typically responds completely to treatment with corticosteroids.
* Class III is focal proliferative nephritis and often successfully responds to treatment with high doses of corticosteroids.
* Class IV is diffuse proliferative nephritis. This form is mainly treated with corticosteroids and immunosuppressant drugs.
* Class V is membranous nephritis and is characterized by extreme edema and protein loss.
The medical therapy for lupus nephritis depends on the severity of the disease. For mild disease, corticosteroids are, in general, prescribed. More severe disease requires treatment with immunosuppressant agents. The two most commonly-used agents are mycophenolate mofetil and intravenous cyclophosphamide.
The differential diagnosis for neonatal seizures is voluminous. Important causes include the following:
* Seizures resulting from hypoxic-ischemic encephalopathy may be seen in both term and premature infants. They frequently present within the first 72 hours of life. Seizures may include subtle, clonic, or generalized seizures.
* Intracranial hemorrhage occurs more frequently in premature than in term infants. Distinguishing infants with pure hypoxic-ischemic encephalopathy from those with intracranial hemorrhage often is difficult.
Metabolic disturbances include hypoglycemia, hypocalcemia, and hypomagnesemia. Less frequent metabolic disorders, such as inborn errors of metabolism, are seen more commonly in infants who are older than 72 hours. Typically, they may be seen after the infant starts feeding.
Intracranial infections (which should be ruled out vigorously) that are important causes of neonatal seizures include meningitis, encephalitis (including herpes encephalitis), toxoplasmosis, and cytomegalovirus (CMV) infections. The common bacterial pathogens include Escherichia coli and Streptococcus pneumoniae.
While most cerebral malformations present with seizures at a later age, major malformation syndromes are important to consider. Lissencephaly, pachygyria, polymicrogyria, and linear sebaceous nevus syndrome can present with seizures in the neonatal period.
Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow
-- bleeding: trauma, GI bleeding, ruptured aneurysms, hemorrhagic pancreatitis
-- protracted vomiting or diarrhea
-- adrenal insufficiency; diabetes insipidus
-- third spacing: intestinal obstruction, pancreatitis, cirrhosis
Mechanism: release of inflammatory mediators leading to
Disruption of the microvascular endothelium
Cutaneous arteriolar dilation and sequestration of blood in cutaneous venules and small veins
Anaphylaxis, drug, toxin reactions
Trauma: crush injuries, major fractures, major burns.
infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis, meningitis, cholangitis, pyelonephritis, necrotic tissue, pancreatitis, wet gangrene, toxic shock syndrome, etc.
Mechanism: Intrinsic abnormality of heart -> inability to deliver blood into the vasculature with adequate power
Cardiomyopathies: myocardial ischemia, myocardial infarction, cardiomyopathy, myocardiditis, myocardial contusion
Mechanical: cardiac valvular insufficiency, papillary muscle rupture, septal defects, aortic stenosis
Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrial fibrillation, atrial flutter, ventricular fibrillation)
Obstructive disorders: PE, tension peneumothorax, pericardial tamponade, constrictive pericaditis, severe pulmonary hypertension
Characterized by high preload (CVP) with low CO
Signs/SXS: Dyspnea, rales, loud P2 gallop, low BP, oliguria
Monitor/findings: CXR pulm venous congestion, elevated CVP, Low CO.
The most common causes of CKD are diabetes mellitus, hypertension, and glomerulonephritis.Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy.
Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products.Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis shows that the kidney is allowing the loss of protein or red blood cells into the urine.To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy are employed to find out if there is a reversible cause for the kidney malfunction.Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD).
There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a kidney transplant.
Risk factors for the development of meningitis include low birth weight (<2500 g), preterm birth (<37 weeks' gestation), premature rupture of membranes, traumatic delivery, fetal hypoxia, and maternal peripartum infection (including chorioamnionitis).
Early onset bacterial meningitis,
* Symptoms appearing in the first 48 hours of life are referable primarily to systemic illness rather than meningitis. These include temperature instability, episodes of apnea or bradycardia, hypotension, feeding difficulty, hepatic dysfunction, and irritability alternating with lethargy.
Late onset bacterial meningitis,
* Late-onset bacterial meningitis (symptom onset beyond 48 hours of life) is more likely to be associated with neurologic symptoms.Between 25% and 50% of neonates will exhibit the following neurological signs: seizures; bulging anterior fontanel; extensor posturing/ opisthotonus; focal cerebral signs including gaze deviation and hemiparesis; cranial nerve palsies. Nuchal rigidity per se is the least common neurologic sign in neonatal bacterial meningitis.
Four Mechanisms of Arrhythmia
Reentry (most common)
2 distinct pathways that come together at beginning and end to form a loop.
A unidirectional block in one of those pathways.
Slow conduction in the unblocked pathway.
An arrhythmia is triggered by a premature beat
The fast conducting pathway is blocked because of its long refractory period so the beat can only go down the slow conducting pathway
The wave of excitation from the premature beat arrives at the distal end of the fast conducting pathway, which has now recovered and therefore travels retrogradely (backwards) up the fast pathway
On arriving at the top of the fast pathway it finds the slow pathway has recovered and therefore the wave of excitation ‘re-enters’ the pathway and continues in a ‘circular’ movement. This creates the re-entry circuit
Heart cells other than those of the SA node depolarize faster than SA node cells, and take control as the cardiac pacemaker.
Parasystole is a benign type of automaticity problem that affects only a small region of atrial or ventricular cells.
is like a domino effect where the arrhythmia is due to the preceding beat.
Delayed after-depolarizations arise during the resting phase of the last beat and may be the cause of digitalis-induced arrhythmias.
Early after-depolarizations arise during the plateau phase or the repolarization phase of the last beat and may be the cause of torsades de pointes (ex. Quinidine induced)
DIC can occur in the following conditions:
Cancers of lung, pancreas, prostate and stomach, as well as acute myeloid leukemia (particularly APML)
Obstetric: abruptio placentae, pre-eclampsia, amniotic fluid embolism
Massive tissue injury: Trauma, burns, extensive surgery
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
Diagnosis is usually suggested by following conditions:
Severe cases with hemorrhage: The PT and APTT are usually very prolonged and the fibrinogen level markedly reduced. High levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activity stimulated by the presence of fibrin in the circulation. There is severe thrombocytopenia. The blood film may show fragmented red blood cells.
The only effective treatment is the reversal of the underlying cause. Anticoagulants are given exceedingly rarely when thrombus formation is likely to lead to imminent death. 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 anti-thrombotic factors, although these are only temporizing measures and may result in the increased development of thrombosis.
Management Options for patients with BPO
5 α reductase inhibitors:
Alpha- blockers:Trazosin (Itrin),Doxazosin (Cardura),Alfuzosin (Xatral).,Tamsulosin (Flomax, Omnic)
Surgical Therapy of BPO
Transurethral resection of the Prostate (TURP) using a standard wire loop and electrosurgical unit is still regarded as the “Gold Standard” in the treatment of men with BPO
Transurethral vaporization of the prostate (TUVP)
Rolling cylinder (The Vaportrode) provides enhanced contact with prostatic tissue using augmented electrocutting energy.Electrovaporization current maintained efficacy of TURP with minimal bleeding and electrolyte disturbances.
Disadvantages: Slow and Lack of prostatic tissue for histopathological examination.
Orbital floor fractures can increase volume of the orbit with resultant hypoglobus and enophthalmos.The inferior rectus muscle or orbital tissue can become entrapped within the fracture, resulting in tethering and restriction of gaze and diplopia.
Significant orbital emphysema from a communication with the maxillary sinus can occur. Orbital hemorrhage is possible with risk of a compressive optic neuropathy.
The globe can be ruptured or suffer less severe forms of trauma, resulting in hyphema, retinal edema, and profound visual loss.
Periorbital ecchymosis and edema accompanied by pain are obvious external signs and symptoms, respectively. Enophthalmos is possible but initially can be obscured by surrounding tissue swelling. This swelling can restrict ocular motility, giving the impression of soft tissue or inferior rectus entrapment. Retrobulbar or peribulbar hemorrhage may be heralded by proptosis. A bony step-off of the orbital rim and point tenderness are possible during palpation.
Examination of the globe is essential, albeit difficult because of soft tissue edema. Desmarres retractors may be helpful to spread edematous eyelids.
Pupillary dysfunction coupled with decreased visual acuity should alert one to the possibility of a traumatic or compressive optic neuropathy.Ocular misalignment, hypotropia or hypertropia, and limitation of elevation ipsilateral to the fracture are possible. Forced duction testing can differentiate entrapment versus neuromyogenic etiologies of muscle underaction.The supratarsal crease may deepen, along with narrowing of the palpebral fissure stemming from enophthalmos or fibrous tissue contraction. Although the palpebral fissure may in fact narrow, the geometric shape is preserved, since dehiscence or disruption of the canthal tendons is uncommon.
SARS may be suspected in a patient who has:
1. Any of the symptoms, including a fever of 38 °C (100.4 °F) or higher, and
2. Either a history of:
1. Contact (sexual or casual) with someone with a diagnosis of SARS within the last 10 days OR
2. Travel to any of the regions identified by the WHO as areas with recent local transmission of SARS
A probable case of SARS has the above findings plus positive chest X-ray findings of atypical pneumonia or respiratory distress syndrome.White blood cell and platelet counts are often high.
Three possible diagnostic tests have emerged, each with drawbacks. The first, an ELISA (enzyme-linked immunosorbent assay) test detects antibodies to SARS reliably but only 21 days after the onset of symptoms. The second, an immunofluorescence assay, can detect antibodies 10 days after the onset of the disease but is a labour and time intensive test, requiring an immunofluorescence microscope and an experienced operator. The last test is a polymerase chain reaction (PCR) test that can detect genetic material of the SARS virus in specimens ranging from blood, sputum, tissue samples and stools. The PCR tests so far have proven to be very specific but not very sensitive.M
No clear evidence that treatment of thyroid cancers of < 1 cm alters life expectancy
Most thyroid cancers: papillary or follicular histology with excellent prognosis
Risk of malignancy greater for patients < 20 years and > 60 years of age
Higher risk with previous radiation exposure
Cancer risk of 10 - 13% whether thyroid contains solitary or multiple nodules
US Features of Malignant Thyroid Nodules
Taller than wide
Marked hypoechogenicity (less than adjacent strap muscles)
Coarse internal calcifications
Internal blood flow
Annual incidence rates of microalbuminuria of 1% to 2% are reported consistently for both type 1 and type 2 diabetes
Moreover, diabetes accounts for 45% of prevalent kidney failure, up from 18% in 1980.
Diabetic Kidney Disease (CKD)
Although kidney biopsy is required to diagnose diabetic glomerulopathy definitively, in most cases, careful screening of diabetic patients can identify people with DKD
DKD is based in part on the finding of elevated urinary albumin excretion, which is divided arbitrarily into: microalbuminuria, a modest elevation of albumin thought to be associated with stable kidney function, but a greater risk of macroalbuminuria and kidney failure
macroalbuminuria, a higher elevation of albumin associated with progressive decline in glomerular filtration rate (GFR), an increase in systemic blood pressure, and a high risk of kidney failure.
An elevated ACR should be confirmed in the absence of urinary tract infection with 2 additional first-void specimens collected during the next 3 to 6 months.
Microalbuminuria is defined as an ACR between 30-300 mg/g.
Macroalbuminuria is defined as an ACR > 300 mg/g.
2 of 3 samples should fall within the microalbuminuric or macroalbuminuric range to confirm classification.
In most patients with diabetes, CKD should be attributable to diabetes if:
Macroalbuminuria is present; or
Microalbuminuria is present
In the presence of diabetic retinopathy
In type 1 diabetes of at least 10 years' duration.
Although no-one has identified the cause of Perthes disease it is known that there is a reduction in blood flow to the joint. It is thought that the artery of the ligamentum teres femoris closes too early, not allowing time for the medial circumflex femoral artery to take over.
Common symptoms include hip, knee, or groin pain, exacerbated by hip/leg movement. The pain feels like a tooth ache, possibly severe. There is a reduced range of motion at the hip joint and a painful or antalgic gait. There may be atrophy of thigh muscles from disuse and an inequality of leg length. In some cases, some activity can cause severe irritation or inflammation of the damaged area including standing, walking, running, kneeling, or stooping repeatedly for an extended period of time.
X-Rays of the hip confirm the diagnosis. X-rays usually demonstrates a flattened and later fragmented head of femur. A bone scan or MRI may be useful in making the diagnosis in those cases where x-rays are inconclusive. Neither bone scan or MRI offer any additional useful information beyond that of x-rays in an established case.
The goal of treatment is to avoid severe degenerative arthritis. Orthopedic assessment is crucial. Younger children have a better prognosis than older children.
The main symptom is pain,causing loss of ability and often stiffness."Pain" is generally described as a sharp ache, or a burning sensation in the associate muscles and tendons. OA can cause crepitus when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. OA is the most common cause of joint effusion, sometimes called water on the knee in lay terms, an accumulation of excess fluid in or around the knee joint.
OA commonly affects the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.
In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen. Some people notice these physical changes before they experience any pain.
Brain is protected by cranial bones, cranial meninges, and CSF.
Brain stem consists of the medulla oblongata, pons, and midbrain. Lower end is a continuation of the spinal cord.
Diencephalon consists primarily of the thalamus and hypothalamus.
Cerebrum spreads over the diencephalon and occupies most of the cranium.
Inferior to the cerebrum and posterior to the brain stem is the cerebellum.
Cranial meninges surround the brain and are continuous with the spinal meninges.
Tough fibrous structure containing an inner (meningeal) layer and outer (periosteal) layer
Most of the dura’s venous sinuses lie between the dural layers
Dural layers are generally fused, except where they separate to provide space for the venous sinuses and where the inner layer forms septa between the brain portions
Outer layer firmly attached to inner surface of cranial bones; inner layer continuous with spinal dura
Delicate avascular membrane covers the subarachnoid space
Between the arachnoid and dura mater lies the subdural space
Arachnoid granulations project into the superior sagittal sinus
Subarachnoid space between the arachnoid and the pia is relatively narrow over the surface of the cerebral hemisphere and is much wider at areas at the base of the brain
Thin connective tissue membrane that covers the brain surface and extends into sulci and fissures and around blood vessels throughout the brain
Invaginations of the pia form choroid plexuses of the ventricles
Various types of lesions, malformations, or pathology may present in one or more intracranial compartments
Occurs in 1-2% of patients with pulmonary TB
One Spanish study found 4.4% of pulmonary TB patient s had pericarditis
Keep in mind that Spanish (and South African) figures on incidence far exceed that in the USA
A Mayo clinic study found 2% cases of pericarditis in pulmonary TB patients as apposed to a similar study at Mayo fifty years ago
However, parts of the USA have high immigrant populations where TB pericarditis rates are much higher, as established at Baylor in 1990.
TB pericarditis is usually associated with TB somewhere else in body
Usually represent reactivation disease thus a primary infective location usually not found
Do not necessarily occur in order or individually
Inflammatory process thought secondary to hypersensitivity reaction to tuberculoprotein
Serosangiouness fluid with leukocytes and high protein and tubercle bacilli found in low concentration
Pressures consistent with cardiac tamponade are found
Pericarditis caused by tuberculosis is difficult to diagnose, because definitive diagnosis requires culturing Mycobacterium tuberculosis from aspirated pericardial fluid or pericardial biopsy, which requires high technical skill and is often not diagnostic (the yield from culture is low even with optimum specimens). The Tygerberg scoring system helps the clinician to decide whether pericarditis is due to tuberculosis or whether it is due to another cause
* Stress incontinence, also known as effort incontinence, is due essentially to insufficient strength of the pelvic floor muscles.
* Urge incontinence is involuntary loss of urine occurring for no apparent reason while suddenly feeling the need or urge to urinate.
* Overflow incontinence: Sometimes people find that they cannot stop their bladders from constantly dribbling, or continuing to dribble for some time after they have passed urine. It is as if their bladders were like a constantly overflowing pan, hence the general name overflow incontinence.
* Polyuria - uncontrolled diabetes mellitus,central diabetes insipidus and nephrogenic diabetes insipidus.
* Caffeine stimulates the bladder.
* Enlarged prostate is the most common cause of incontinence in men after the age of 40; sometimes prostate cancer may also be associated with urinary incontinence. Moreover drugs or radiation used to treat prostate cancer can also cause incontinence.
* Brain disorders like multiple sclerosis, Parkinson's disease, strokes and spinal cord injury can all interfere with nerve function of the bladder.
Orotracheal Intubation- preferred in almost all situations
present or impending respiratory failure
unable to protect own airway (<8)
route for a few medications
optimizes ventilation and oxygenation
Nasotracheal Intubation- rarely if ever used in the initial management of the injured patient.
Goal of safe endotracheal intubation with cervical spine precautions can be better accomplished with orotracheal intubation
absolute need for a definitive airway AND
unable to perform ETT due for structural or anatomic reasons, AND
risk of not intubating is > surgical airway risk
absolute need for a definitive airway AND
unable to clear an upper airway obstruction, AND
multiple unsuccessful attempts at ETT, AND
other methods of ventilation do not allow for effective ventilation and respiration
Age < 8 years (some say 10)
evidence of fx larynx or cricoid cartilage
evidence of tracheal transection
Needle Cricothyrotomy & Transtracheal Jet Ventilation
Same as surgical cricothyrotomy along with
Contraindication for surgical cricothyrotomy
caution with tracheal transection
Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time.As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (ocular hemorrhage) and blur vision. The first time this happens, it may not be very severe. In most cases, it will leave just a few specks of blood, or spots, floating in a person's visual field, though the spots often go away after a few hours.
On funduscopic exam, a doctor will see cotton wool spots, flame hemorrhages and dot-blot hemorrhages.
As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage when blood vessels proliferate.The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina. Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.
Photosensitivity's relationship to and influence on the systemic manifestations of lupus remain to be defined. Mechanisms for photosensitivity might include: modulation of autoantibody location, cytotoxic effects, apoptosis induction with autoantigens in apoptotic blebs, upregulation of adhesion molecules and cytokines, induction of nitric oxide synthase expression and ultraviolet-generated antigenic DNA. Tumor necrosis factor alpha also seems to play a role in the development of photosensitivity.
Aside from intellectual disability, prominent characteristics of the syndrome include an elongated face, large or protruding ears, flat feet, larger testes (macroorchidism), and low muscle tone. Speech may include cluttered speech or nervous speech.Behavioral characteristics may include stereotypic movements (e.g., hand-flapping) and atypical social development, particularly shyness, limited eye contact, memory problems, and difficulty with face encoding.
Fragile X syndrome was originally diagnosed by culturing cells in a folate deficient medium and then assessing the cultures for X-chromosome breakage by cytogenetic analysis of the long arm of the X chromosome. This technique proved unreliable for both diagnosis and carrier testing.
The fragile X abnormality is now directly determined by analysis of the number of CGG repeats and their methylation status using restriction endonuclease digestion and Southern blot analysis.
Fragile X syndrome is an X-linked dominant condition with variable expressivity and possibly reduced penetrance.Because males normally have only one copy of the X chromosome, those males with significant trinucleotide expansion at the FMR1 locus are symptomatic. Females have two X chromosomes and thus have an increased probability of having a working FMR1 allele. Females carrying one X chromosome with an expanded FMR1 gene can have some signs and symptoms of the disorder or be normal.
Fractures around the trunk are often complicated by visceral injury. E.g. Rib fractures are associated with life threatening pneumothorax or with spleen, liver injuries. E.g. Pelvic injuries are associated with bladder or urethral rupture and cause sever hematoma in the retroperitoneum .Surgery of visceral injuries should take precedence over the treatment of fracture.
Most associated with injuries around knee, elbow, humerus and femoral shaft.
Commonly associated with high-energy open fractures.
They are rare but well-recognized.
Cause : From initial trauma or from bone fragment
Mechanism of injuries:
** The artery may be cut or torn.
** Compressed by the fragment of bone.
** normal appearance with intimal detachment that lead to thrombus formation.
** segment of artery may be in spasm.
Classical presentation of ischemia 5 Ps: Pain , Pallor, Pulseless , Paralysis , and Paraesthesia
X-ray: suggest high-risk fracture. Angiogram should be performed to confirm diagnosis.
This is an emergency because the effect of ischemia especially on the muscle is irrevesible after 6 hours.
1. Temporary vascular shunt to perfuse distal limb.
2. Skeletal stabilization – temporary external fixation often used.
3. Definitive vascular repair.
4. Staged definitive skeletal internal fixation if required.
- It’s more common than arterial injuries. - The most commonly injured nerve is the radial nerve in its groove or in the lower third of the upper arm especially in oblique fracture of the humerus. - Common with humerus, elbow and knee fractures - Most nerve injuries are due to tension neuropraxia.
**Most commonly in forearm and calfs. **Muscles are arranged in different compartments and surrounded by one fascia , this arrangement called osteofascial compartment. **Compartment syndrome occurs when muscle swells within osteofacial compartment and occluds its blood supply >infarction and late ischemic contracture. **Trauma is the most common cause. reasons that lead to increase the pressure inside: 1. Bleeding 2. Edema 3. Infection
A lesion which projects into the lumen of the bowel.
Size of a few mm to several cm in diameter.
Single or multiple. In polyposis syndrome hundreds may be found
Larger polyps are found in the rectum
5% may contain invasive carcinoma at discovery
The type of cell that forms the polyp varies and is important in determining its potential for developing into a cancer
Most polyps are asymptomatic until they grow to 2cm in diameter
They can lead to bleeding, frank blood or microscopic bleeding (presenting with anaemia)
Polyps rarely present with a change in bowel habit – but large polyps in the rectum can present with tenesmus.
A large amount of mucus can also be passed.
Rarely a polyp will prolapse through the anus or act as an apex for an intussception.
Classification of polyps
Familial adenomatous polyposis (FAP)
Protrusions of mesenchymal tissue
Pseudopolyps in Ulcerative colitis
Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low PaCO2. This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units.
Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders.