Alcohol binge: vodka
Awake and conversant
Severe abdominal pain, vomiting, dyspnoea
Physical and laboratory examinations
Pulse 96 bpm, respirations 20/min
Blood pressure 110/70 mmHg
Abdomen tender, distended, quiet
Amylase 3500 IU/L
Lipase 1100 IU/L
AST >250 IU/L
LDH >350 IU/L
WBC count 16 000/mm3
Arterial blood gases:
pH 7.30, PaCO2 32, PaO2 58, BE -5
Which evaluations would you perform to determine if the patient has severe pancreatitis?
Computed tomography (CT) scan
Glasgow (Imrie) score
APACHE II or III score
Molar pregnancies are an uncommon and very serious complication of pregnancy. The formal medical term for a molar pregnancy is “hydatidiform mole.” Simply put, a molar pregnancy is an abnormality of the placenta,caused by a problem when the egg and sperm join together at fertilization.
The incidence of molar pregnancy varies depending on where one lives. For example, in the US about 1 out of every 1000 pregnancies is a molar pregnancy. In Southeast Asia the incidence is 8 times higher. Age over 40 is a risk factor for molar pregnancy, as is having a prior molar pregnancy.
Women with a molar pregnancy usually feel pregnant and complain of vaginal spotting or bleeding. Many women with molar pregnancies develop nausea and vomiting. Some even develop rare complications like thyroid disease or very early preeclampsia (toxemia). Preeclampsia occurring earlier than 20 weeks is very worrisome for a molar pregnancy. The ultrasound will often show a “cluster of grapes” appearance or a “snowstorm” appearance, signifying an abnormal placenta. If a baby is present it’s a possible partial mole, while if the baby is absent it’s probably a complete mole. Treatment consists of a D&C (dilation and curettage) of the uterus, where a small vacuum device is inserted into the uterus, under anesthesia, to remove the molar pregnancy. This must be done very carefully or excessive bleeding and blood clots to the lungs can occur.
Rhabdomyolysis may be caused by any one of a variety of means. Essentially, any situation causing muscle tissue destruction has the potential to be a rhabdomyolysis cause. These are considered to be either physical or non-physical causes. Rhabdomyolysis brought on by physical causes tends to be restricted to one region of the patient's body, whereas non-physical rhabdomyolysis typically harms all of the body's muscles at once.
Physical rhabdomyolysis causes
Traumatic muscle compression - car accident, crush syndrome,physical abuse, etc.
Blood supply to muscle obstruction - arterial thrombosis, artery clamping, embolism, reduced blood supply (in shock or sepsis), etc.
Excessive activity in muscles - Alcohol withdrawal (delirium tremens), extreme physical exercise,persistent seizures (status epilepticus, SE), tetanus, etc.
Electrical shock - high voltage electric shock
Non-physical rhabdomyolysis causes
Autimmune muscle damage - dermatomyositis, polymyositis, etc.
Disturbances of electrolytes or metabolism - hypernatremia and hyponatremia, hypocalcemia , hypokalemia, hypophosphatemia, hypothyroidism, increased plasma osmolality, ketoacidosis, etc.
Infections - Coxsackie virus, herpes virus, Legionella pneumophila, malaria (Plasmodium falciparum), Salmonella, tularemia (Francisella tularensis), etc.
Muscle energy supply disorders - carnitine palmitoyltransferase I deficiency or carnitine palmitoyltransferase I deficiencyprimary carnitine deficiency (CPT type I or II), McArdle's disease, mitochondrial respiratory chain defects, phosphofructokinase deficiency, primary carnitine deficiency, VLCAD deficiency, etc.
Prolonged seizures are associated with cerebral hypoxia, hypoglycemia, and hypercarbia and with concurrent and progressive lactic and respiratory acidosis. When cerebral metabolic needs exceed available oxygen, glucose, and metabolic substrates (especially during status epilepticus), neuronal destruction can occur and may be irreversible.
Causes of Status epilepticus in Children
* Birth injury (eg, anoxia, hemorrhage) and congenital abnormalities
* Metabolic disorders (eg, hypoglycemia, hypocalcemia, hyponatremia) and inborn errors of metabolism (eg, lipidoses, amino acidurias)
* Infection (eg, meningitis)
* Birth injury
* Febrile convulsions (3 mo to 6 y)
* Metabolic disorders
* Neurocutaneous syndromes
* Cerebral degenerative diseases
Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves. There is oversecretion of PTH due to adenoma, hyperplasia or, rarely, carcinoma of the parathyroid glands.
Secondary hyperparathyroidism is the reaction of the parathyroid glands to a hypocalcemia caused by something other than a parathyroid pathology, e.g. chronic renal failure.
Tertiary hyperparathyroidism result from hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with chronic renal failure and is an autonomous activity.
Most of the symptoms of parathyroid disease are "neurological" in origin. Common manifestations of hyperparathyroidism include weakness and fatigue, depression, bone pain, muscle soreness (myalgias), decreased appetite, feelings of nausea and vomiting, constipation, polyuria, polydipsia, cognitive impairment, kidney stones and osteoporosis.
Osteomalacia associated with hyperparathyroidism is caused by the high parathyroid hormone secreted by overactive parathyroid gland.
The causes for upper GI hemorrhage include the following:
* Esophageal causes:Esophageal varices,Esophagitis,Esophageal cancer,Mallory-Weiss tear
* Gastric causes:Gastric ulcer,Gastric cancer,Gastric varices,Gastric antral vascular ectasia,Dieulafoy's lesions
*Vascular malformation, including aorto-enteric fistulae.
*Severe superior mesenteric artery syndrome
Emergency treatment for upper GI bleeds includes aggressive replacement of volume with intravenous solutions, and blood products if required. As patients with esophageal varices typically have coagulopathy, plasma products may have to be administered. Vital signs are continuously monitored.Early endoscopy is recommended, both as a diagnostic and therapeutic approach, as endoscopic treatment can be performed through the endoscope.
Type I - Collagen is of normal quality but is produced in insufficient quantities:
* Bones fracture easily
* Slight spinal curvature
* Loose joints
* Poor muscle tone
* Discoloration of the sclera (whites of the eyes), usually giving them a blue-gray color
Type II - Collagen is not of a sufficient quality or quantity
* Most cases die within the first year of life due to respiratory failure or intracerebral hemorrhage
Type III- Collagen improperly formed. Enough collagen is made but it is defective
* Bones fracture easily, sometimes even before birth
* Bone deformity, often severe
* Respiratory problems possible
* Short stature, spinal curvature and sometimes barrel-shaped rib cage
Type IV - Collagen quantity is sufficient but is not of a high enough quality
Type V - Same clinical features as Type IV
There have been many clinical trials performed with Fosamax (Alendronate), a drug used to treat those experiencing brittleness of bones due to osteoporosis. Higher levels of effectiveness apparently are to be seen in the pill form versus the IV form, but results seem inconclusive.Bone infections are treated as and when they occur with the appropriate antibiotics and antiseptics.
Invasive cancers that are confined within the wall of the colon (TNM stages I and II) are curable with surgery. If untreated, they spread to regional lymph nodes (stage III), where up to 73% are curable by surgery and chemotherapy. Cancer that metastasizes to distant sites (stage IV) is usually not curable, although chemotherapy can extend survival, and in rare cases, surgery and chemotherapy together have seen patients through to a cure.Radiation is used with rectal cancer.
The symptoms of colorectal cancer depend on the location of tumor in the bowel, and whether it has spread elsewhere in the body.Most of the symptoms may occur in other diseases as well, and hence none of the symptoms mentioned here is diagnostic of colorectal cancer.Symptoms and signs are divided into local, constitutional and metastasizes.
Local symptoms are more likely if the tumor is located closer to the anus. There may be a change in bowel habit and a feeling of incomplete defecation (rectal tenesmus) and change in stool shape is characteristic of rectal cancer.Lower gastrointestinal bleeding, including the passage of bright red blood in the stool, may indicate colorectal cancer, as may the increased presence of mucus. Melena, black stool with a tarry appearance, normally occurs in upper gastrointestinal bleeding,but is sometimes encountered in colorectal cancer when the disease is located in the beginning of the large bowel.
A tumor that is large enough to fill the entire lumen of the bowel may cause bowel obstruction. This situation is characterized by constipation, abdominal pain, abdominal distension and vomiting. This occasionally leads to the obstructed and distended bowel perforating and causing peritonitis. A large left colonic tumor may compress the left ureter and cause hydronephrosis.
Certain local effects of colorectal cancer occur when the disease has become more advanced. A large tumor is more likely to be noticed on feeling the abdomen, and it may be noticed by a doctor on physical examination. The disease may invade other organs, and may cause blood or air in the urine (invasion of the bladder) or vaginal discharge (invasion of the female reproductive tract).If a tumor has caused chronic occult bleeding, iron deficiency anemia may occur; this may be experienced as fatigue, palpitations and noticed as pallor (pale appearance of the skin). Colorectal cancer may also lead to weight loss, generally due to a decreased appetite.More unusual constitutional symptoms are an unexplained fever and one of several paraneoplastic syndromes.
American Heart Association Guidelines for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care
• A compression rate of at least 100/min (a change from “approximately” 100/min)
• A compression depth of at least 2 inches (5 cm) in adults and a compression depth of at least one third of the anteriorposterior diameter of the chest in infants and children(approximately 1.5 inches [4 cm] in infants and 2 inches[5 cm] in children). Note that the range of 1½ to 2 inches is no longer used for adults, and the absolute depth specified for children and infants is deeper than in previous versions of the AHA Guidelines for CPR and ECC
Allowing for complete chest recoil after each compression
• Minimizing interruptions in chest compressions
• Avoiding excessive ventilation
There has been no change in the recommendation for a compression-to-ventilation ratio of 30:2 for single rescuers of adults, children, and infants (excluding newly born infants). The 2010 AHA Guidelines for CPR and ECC continue to recommend
that rescue breaths be given in approximately 1 second. Once an advanced airway is in place, chest compressions can be continuous (at a rate of at least 100/min) and no longer cycled with ventilations. Rescue breaths can then be provided at about 1 breath every 6 to 8 seconds (about 8 to 10 breaths per minute). Excessive ventilation should be avoided.
Hyponatremia is an electrolyte disturbance in which the sodium concentration in the serum is lower than normal.Normal serum sodium levels are between 135-145 mEq/L. Hyponatremia is defined as a serum level of less than 135 mEq/L and is considered severe when the serum level is below 125 mEq/L. Sodium is the dominant extracellular cation and cannot freely cross the cell membrane. Its homeostasis is vital to the normal physiologic function of cells.
Criteria for SIRS were established as part of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference.The conference concluded that the manifestations of SIRS include, but are not limited to:
* Body temperature less than 36°C or greater than 38°C
* Heart rate greater than 100 beats per minute
* Tachypnea with greater than 20 breaths per minute; or, an arterial partial pressure of carbon dioxide less than 32 mmHg
* White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109 cells/L); or the presence of greater than 10% immature neutrophils (band forms)
SIRS can be diagnosed when two or more of these criteria are present.
Fever and leukocytosis are features of the acute-phase reaction, while tachycardia is often the initial sign of hemodynamic compromise. Tachypnea may be related to the increased metabolic stress due to infection and inflammation.SIRS is frequently complicated by failure of one or more organs or organ systems.The complications of SIRS include:
* Acute lung injury
* Acute kidney injury
* Multiple organ dysfunction syndrome
Excessive alcohol use is the most common cause of chronic pancreatitis and can also be a contributing factor in acute pancreatitis.
Less common causes are
* viral infection (e.g. mumps),
* trauma (to the abdomen or elsewhere in the body) including post-ERCP
* autoimmune pancreatitis.
* Pancreas divisum, a common congenital malformation of the pancreas
The diagnostic criteria for pancreatitis are "two of the following three features: abdominal pain characteristic of acute pancreatitis, serum amylase and/or lipase ≥3 times the upper limit of normal and characteristic findings of acute pancreatitis on CT scan.
Several scoring systems are used to help predict the severity of an attack of pancreatitis. The Apache II system has the advantage of being available at the time of admission as opposed to 48 hours later as is the case for the Glasgow criteria and Ranson criteria systems .
The usual outcome is poor, because only 10 - 20% of hepatocellular carcinomas can be removed completely using surgery. If the cancer cannot be completely removed, the disease is usually deadly within 3 to 6 months.This is partially due to late presentation with large tumours, but also the lack of medical expertise and facilities. This is a rare tumor in the United States.
Generalized hypoxia occurs in healthy people when they ascend to high altitude, where it causes altitude sickness leading to potentially fatal complications: high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE).Hypoxia also occurs in healthy individuals when breathing mixtures of gases with a low oxygen content, e.g. while diving underwater especially when using closed-circuit rebreather systems that control the amount of oxygen in the supplied air. A mild and non-damaging intermittent hypoxia is used intentionally during altitude trainings to develop an athletic performance adaptation at both the systemic and cellular level.
The symptoms of generalized hypoxia depend on its severity and acceleration of onset. In the case of altitude sickness, where hypoxia develops gradually, the symptoms include headaches, fatigue, shortness of breath, a feeling of euphoria and nausea. In severe hypoxia, or hypoxia of very rapid onset, changes in levels of consciousness, seizures, coma, priapism, and death occur. Severe hypoxia induces a blue discolouration of the skin, called cyanosis.
Frequency = voiding too often
Urgency = sudden compelling desire to pass urine which is difficult to defer
Incontinence = involuntary urine leakage accompanied by or immediately preceded by urgency, and
Nocturia = wake at night one or more times to void
Urge Urinary Incontinence
Unwanted urine leakage after sudden, intense desire to urinate.
Caused by involuntary detrusor contractions as bladder fills.
Unable to prevent urine flow with the “urge” sensation.
Stress Urinary Incontinence
Increased abdominal pressure (eg lifting, coughing) causing involuntary urine leakage.
Poor urethral support.
Predominately in women after child birth.
Failure to store urine due to increased detrusor contractility.
Usually neurological component although can be non-neurological.
Urodynamically defined condition.
In healthy adults, there are two normal heart sounds often described as a lub and a dub,that occur in sequence with each heart beat. These are the first heart sound (S1) and second heart sound (S2), produced by the closing of the AV valves and semilunar valves respectively. In addition to these normal sounds, a variety of other sounds may be present including heart murmurs, adventitious sounds, and gallop rhythms S3 and S4.
Heart murmurs are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological or pathological.Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (or regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of the murmur.
Regurgitation through the mitral valve is by far the most commonly heard murmur, producing a pansystolic murmur which is sometimes fairly loud to a practiced ear, even though the volume of regurgitant blood flow may be quite small.
Stenosis of the aortic valve is typically the next most common heart murmur, a systolic ejection murmur. This is more common in older adults or in those individuals having a two, not a three leaflet aortic valve.
Most women have some changes in their menstrual periods while using Depo-Provera, including irregular and unpredictable bleeding or spotting, an increase or decrease in menstrual bleeding, or no bleeding at all. After 1 year of use, about 50% of women have no bleeding at all. Other possible side effects include weight gain, headaches, nervousness, abdominal discomfort, dizziness and weakness or fatigue.
*Critical illness (eg, major surgery, burns, sepsis, or trauma)
*Prolonged fasting or TPN (both predispose to bile stasis)
*Vasculitis (eg, SLE, polyarteritis nodosa)
The mechanism probably involves inflammatory mediators released because of ischemia, infection, or bile stasis. Sometimes an infecting organism can be identified (eg, Salmonella sp or cytomegalovirus in immunodeficient patients). In young children, acute acalculous cholecystitis tends to follow a febrile illness without an identifiable infecting organism.
The symptoms are similar to those of acute cholecystitis with gallstones but may be difficult to identify because patients tend to be severely ill (eg, ICU setting) and may be unable to communicate clearly. Abdominal distention or unexplained fever may be the only clue. Untreated, the disease can rapidly progress to gallbladder gangrene and perforation, leading to sepsis, shock, and peritonitis; mortality approaches 65%.
Acute acalculous cholecystitis is suggested if a patient has no gallstones but has ultrasonographic Murphy's sign or a thickened gallbladder wall and pericholecystic fluid. A distended gallbladder, biliary sludge, and a thickened gallbladder wall without pericholecystic fluid (due to low albumin or ascites) may result simply from a critical illness. CT identifies extrabiliary abnormalities. Cholescintigraphy is more helpful; failure of a radionuclide to fill may indicate edematous cystic duct obstruction.
Status epilepticus can be divided into two categories—convulsive and nonconvulsive, the latter of which is underdiagnosed.
Epilepsia partialis continua is a variant involving hour, day, or even week-long jerking. It is a consequence of vascular disease, tumours, or encephalitis, and is drug-resistant.
Generalized myoclonus is commonly seen in comatose patients following CPR and is seen by some as an indication of catastrophic damage to the neocortex.
Complex partial status epilepticus, or CPSE, and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures. In the case of CPSE, the seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, absence status epilepticus, is marked by a generalised seizure affecting the whole brain, and an EEG is needed to differentiate between the two conditions. This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.
The first symptom to develop is usually muscular cramps, fever, symptoms of instability of the autonomic nervous system such as unstable blood pressure, and changes in cognition, including agitation, delirium and coma. Other symptoms may include muscle tremors.A raised white blood cell count and creatine phosphokinase (CPK) plasma concentration will be reported due to increased muscular activity and rhabdomyolysis .The patient may suffer hypertensive crisis and metabolic acidosis.
Differentiating NMS from other neurological disorders can be very difficult.Some of the most commonly mistaken diseases are: encephalitis, toxic encephalopathy, status epilepticus, heat stroke, and malignant hyperthermia.NMS is usually caused by neuroleptic drug use, and a wide range of drug potencies can result in NMS.It has been reported that individuals using haloperidol and chlorpromazine are at greatest risk.
NMS is an emergency, and can lead to death if untreated. The first step is to stop neuroleptic drugs and to treat the hyperthermia aggressively, such as with cooling blankets or ice packs to the axillae and groin. Many cases require intensive care and circulatory and ventilatory support. Medications such as dantrolene sodium and bromocriptine may be used. Apomorphine may be used however its use is supported by little evidence. Benzodiazepines may be used to control agitation. Highly elevated CPK can damage the kidneys, therefore aggressive hydration may be required.
* Inflammatory myopathies, such as dermatomyositis
* Thyroid disorders (specially hypothyroidism)
* Steroids, cushing's disease for example
* Statins therapy
* Myasthenia gravis
Accounts for 3- 10% of medical admissions
Is associated with a 6 fold increase in stroke rate
Is associated with a 2 fold increase in mortality from IHD
Prevalence increases as population ages
An ECG should be performed in all patients
Rate control and rhythm control should not be considered mutually exclusive and appropriate anti thrombotic therapy should be used
In pts with permanent AF Beta blockers/Ca Antagonists should be the preferred initial monotherapy, digoxin should be reserved for those predominantly sedentary
Anti-thrombotic therapy should be initiated with minimal delay
Stroke risk algorithm should be used in pts and app thromboprophylaxis given
Either rhythm or rate control strategy
If decision taken to go for rhythm control treat precipitants first
Electrical vs. pharmacological Cardioversion
No difference between these if duration less 48hrs
If combination used then PCV+ECV more successful than ECV+PCV
If AF of <48hrs Pharmacological Cardioversion If AF of >48hrs then electrical Cardioversion
In the absence of structural heart disease (IHD or LVSD) a class 1c drug such as Flecainide or Propafenone should be drug of choice
In the presence of structural heart disease Amiodarone should be drug of choice
When pts with AF undergo ECV and there is a cause for heightened concern about success of restoring SR (prev failure or early recurrence) then concomitant Amiodarone or Sotolol for 4 weeks should be given...
The key to the successful application of noninvasive ventilation is in recognizing its capabilities and limitations. This also requires identification of the appropriate patient for the application of noninvasive ventilation (NIV). Patient selection is crucial for the successful application of noninvasive ventilation.
Suitable clinical conditions for noninvasive ventilation (most patients)
Chronic obstructive pulmonary disease
Cardiogenic pulmonary edema
Absolute contraindications are
* Cardiac arrest
* Respiratory arrest
* Any condition requiring immediate intubation
The pain can often be divided into neck pain, upper back pain, lower back pain. It may have a sudden onset or can be a chronic pain; it can be constant or intermittent, stay in one place or radiate to other areas. It may be a dull ache, or a sharp or piercing or burning sensation. The pain may radiate into the arm and hand), in the upper back, or in the low back, (and might radiate into the leg or foot), and may include symptoms other than pain, such as weakness, numbness or tingling.
The spine is a complex interconnecting network of nerves, joints, muscles, tendons and ligaments, and all are capable of producing pain. Large nerves that originate in the spine and go to the legs and arms can make pain radiate to the extremities.
The management goals when treating back pain are to achieve maximal reduction in pain intensity as rapidly as possible; to restore the individual's ability to function in everyday activities; to help the patient cope with residual pain; to assess for side-effects of therapy; and to facilitate the patient's passage through the legal and socioeconomic impediments to recovery. For many, the goal is to keep the pain to a manageable level to progress with rehabilitation, which then can lead to long term pain relief. Also, for some people the goal is to use non-surgical therapies to manage the pain and avoid major surgery, while for others surgery may be the quickest way to feel better.
Many medications can injure the kidneys. Dosing schedules can help prevent acute renal failure. For example, acute renal failure is less likely to develop with a once-daily dose of an aminoglycoside than with multiple daily doses.When acute renal failure is diagnosed, the causes must be identified and treated.Critical measures include maintaining adequate intravascular volume and mean arterial pressure, discontinuing all nephrotoxic drugs, and eliminating exposure to any other nephrotoxins.Electrolyte abnormalities must be corrected, and urine output should be monitored closely.
Hyperkalemia is a common complication of acute renal failure.Potassium levels below 6 mEq per L (6 mmol per L) usually can be managed with dietary restriction and resin binders. Sodium bicarbonate therapy should be reserved for the treatment of severe metabolic acidosis with or without associated hyperkalemia.When hyperkalemia is severe and unresponsive to treatment, kidney replacement therapy may be indicated.
Symptoms of kidney stones include:
Localization of kidney stone pain
* Colicky pain: "loin to groin". Often described as "the worst pain ever experienced." This can also occur in the lower back.The pain is elicited by contractions of the ureter in response to the stone, causing severe, crampy pain in the flank or lower back, often radiating to the groin or, in men, to the testes.The pain typically comes in waves, with a typical wave lasting 20 to 60 minutes
* Nausea/vomiting: embryological link with intestine– stimulates the vomiting center.
* Hematuria: blood in the urine, due to minor damage to inside wall of kidney, ureter and/or urethra.
There are several types of kidney stones based on the type of crystals of which they consist. The majority are calcium oxalate stones, followed by calcium phosphate stones. More rarely, struvite stones are produced by urea-splitting bacteria in people with urinary tract infections, and people with certain metabolic abnormalities may produce uric acid stones or cystine stones.
The diagnosis of a kidney stone can be confirmed by radiological studies and/or ultrasound examination; urine tests and blood tests are also commonly performed. When a stone causes no symptoms, watchful waiting is a valid option. In other cases, pain control is the first measure, using for example non-steroidal anti-inflammatory drugs or opioids. Using soundwaves, some stones can be shattered into smaller fragments (this is called extracorporeal shock wave lithotripsy). Sometimes a procedure is required, which can be through a tube into the urethra, bladder and ureter (ureteroscopy), or a keyhole or open surgical approach from the kidney's side. Sometimes, a tube may be left in the ureter (a ureteric stent) to prevent the recurrence of pain. Preventive and structive measures are often advised such as drinking sufficient amounts of water and milk although the effect of many dietary interventions has not been rigorously studied.
The most common reason for admission is respiratory failure and the need for mechanical ventilator.
The vast majority of patients on ventilators require sedation
60-80% of ventilated patients develop delirium at some point during their hospital course
Sedation in Ventilated Patients
Mechanical ventilation is uncomfortable and anxiety provoking
Sedation is often necessary for comfort and airway, line, foley, nursing protection
More than 85% of ventilated patients receive sedation
Benzodiazepines - midazolam, lorazepam, diazepam
Anesthetics - propofol
Special circumstance sedation
Central alpha-agonists - clonidine, dexmedetomidine
Patients exposed to more than one week of high dose opioid or sedative may develop tolerance and/or dependence.
Opioid withdrawal:-Pupillary dilation, sweating, lacrimation, rhinorrhea, yawning, tachycardia, irritability, anxiety
Benzodiazepine withdrawal:-Dysphoria, tremor, headache, nausea, sweating, agitation, anxiety, sleep disturbances, myoclonus, delirium, seizures
Propofol withdrawal not well-described but reported to resemble BZD withdrawal
Staphylococcus aureus, Streptococcus pneumoniae and Streptococcus pyogenes
Pneumococcal pneumonia presents with effusion in 40% patients, empyema occurs only in 5%
Anaerobes and enterobacter are common in mixed infections. Anaerobes are more common after 6 years of age. For anaerobes, aspiration pneumonia is the most common cause followed by lung abscess, sub diaphrag-matic abscess and spreading infection from adjacent sites, e.g. periodontal, retropharyn-geal, peritonsillar and neck abscesses.
Stages of Empyema
Exudative stage (1-3 days)
- Immediate response with outpouring of the fluid.
- Low cellular content
- It is simple parapneumonic effusion with normal pH and glucose levels.
- pH more than 7.30
- glucose more than 60 mg/dl
- pleural fluid/serum glucose ratio more than 0.5
- LDH less than 1000 IU/L
- Gram stain and culture is negative for micro-organism.
Fibrino purulent stage (4 to 14 days)
- Large number of poly-morphonuclear leukocytes and fibrin accumulates
- Fluid pH and glucose level fall while LDH rises.
- Acumulation of neutro-phils and fibrin, effusion becomes purulent and viscous leading to development of empyema.
- There is progressive tendency towards loculations and formation of a limiting membranes.
- Pleural fluid analysis
- Purulent fluid or pH less than 7.10, glucose less than 40 mg/dl and LDH more than 1000 IU/L. Gram stain and culture reports show microorganism.
Organizing stage (after 14 days)
- Fibro-blasts grow into exudates on both the visceral and parietal pleural surfaces
- Development of an inelastic membrane "the peel".
- Thickened pleural peel may prevent the entry of anti-microbial drugs in the pleural space and in some cases can lead to drug resistance.
- Most common in S. aureus infection.
- Thickened pleural peel can restrict lung movement and it is commonly termed as trapped lung
There are many underlying disorders that can cause hemoptysis, ranging from heart problems to trauma to infections to lung disease. Worldwide, tuberculosis is the most common cause of hemoptysis. In industrialized countries, the most common causes are bronchitis, bronchiectasis, and bronchogenic carcinoma.
In patients with AIDS, the most common cause of hemoptysis is pneumonia. In about 15% to 30% of cases, the underlying problem is never found—undiagnosed hemoptysis is commonly referred to as idiopathic hemoptysis.
Classifying hemoptysis as mild or massive (some practitioners classify it as trivial, moderate, or massive) is difficult because the amount of blood is often hard to accurately quantify. Life-threatening, "massive" hemoptysis, which requires immediate medical attention, is differentiated from less severe cases.
Hemoptysis is considered massive, or major, when there is so much blood that it interrupts breathing (generally more than about 200-240 mL, or about 1 cup, in 24 hours). Massive hemoptysis is a medical emergency: the mortality rate for patients with massive hemoptysis can be as high as 75%. Most patients who die from hemoptysis suffer from asphyxiation (lack of oxygen) due to too much blood in the airways.
HIV infection in humans is considered pandemic by the World Health Organization.From its discovery in 1981,AIDS killed more than 25 million people.In 2005, AIDS claimed an estimated 2.4–3.3 million lives, of which more than 570,000 were children. A third of these deaths occurred in Sub-Saharan Africa, retarding economic growth and increasing poverty. At that time, it was estimated that HIV would infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans.Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but routine access to antiretroviral medication is not available in all countries.
HIV infects primarily vital cells in the human immune system such as helper T cells , macrophages, and dendritic cells.HIV infection leads to low levels of CD4+ T cells.When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
Most untreated people infected with HIV-1 eventually develop AIDS.These individuals mostly die from opportunistic infections or malignancies associated with the progressive failure of the immune system.HIV progresses to AIDS at a variable rate affected by viral, host, and environmental factors; most will progress to AIDS within 10 years of HIV infection: some will have progressed much sooner, and some will take much longer.Treatment with anti-retrovirals increases the life expectancy of people infected with HIV.