Hypercapnia (↑ PaCO2)
Respiratory failure manifesting as hypercapnia is known as ventilatory failure.
Signs of ventilatory failure:
 Tachypnea
 Acidemia
 Increased pulsus paradoxus
 Hyperinflation
 Somnolence / Decreased mental status

Hypercapnia - Etiologies
↑VCO2  (Hypermetabolism)
Fever
Seizures
Sepsis
Hyperalimentation

↓VT
Skeletal muscle weakness
Impaired neuromuscular transmission
↓ Lung / chest wall compliance
Airway obstruction
    COPD
    Asthma
    Obstructive sleep apnea

↓RR (Central hypoventilation)
Drugs
Brainstem lesions
Obesity-hypoventilation syndrome

↑VD
Excessive PEEP

Hypercapnia - Treatment
Treat the underlying process
Non-invasive positive pressure ventilation
Intubation and mechanical ventilation

Hypoxia (↓ PaO2)
Respiratory failure manifesting as hypoxia is known as oxygentation failure.
Signs of oxygenation failure:
 Tachypnea
 Alkalemia (acidemia if concurrent ventilatory failure)
 Increased pulsus paradoxus
 Cyanosis
 Agitation --->Somnolence...

SLE Overview_Diagnosis
Diagnosis is clinical and may be made with ≥ 4 classification criteria present
Criteria is (96% specific, 96% sensitive)
any 4 or more of 11 criteria, serially or simultaneously, during any interval of observation
1. malar (butterfly) rash - fixed erythema, flat or raised, over malar eminences, tending to spare nasolabial folds
2. discoid lupus - erythematous raised patches with adherent keratotic scaling and follicular plugging, atrophic scarring may occur
3. photosensitivity - skin rash resulting from unusual reaction to sunlight
4. oral or nasopharyngeal ulcers - usually painless, observed by physician
5. non-erosive arthritis - involving 2 or more peripheral joints with tenderness, swelling or effusion
6. serositis - pleuritis (pleuritic pain, pleuritic rub or pleural effusion) or pericarditis (on ECG, rub or pericardial effusion)
7. renal involvement - persistent proteinuria (> 500 mg/day or 3+ on dipstick) or cellular casts (red cell, hemoglobin, granular, tubular or mixed)
8. seizures or psychosis without other organic cause
9. hematologic disorder
hemolytic anemia with reticulocytosis, OR
WBC < 4,000 at least 2 times, OR
absolute lymphocyte count < 1,500/mm3 at least 2 times, OR
platelet count < 100,000/mm3 without thrombocytopenic drugs
10. immunologic disorder
anti-DNA, antibody to dsDNA [native DNA] in abnormal titer, OR
anti-Sm Ab (antibody to Sm nuclear antigen), OR
positive finding of antiphospholipid antibodies based on
abnormal serum level of IgG or IgM anticardiolipin antibodies, OR
positive test for lupus anticoagulant using standard method, OR
false positive serologic test for syphilis for at least 6 months and confirmed by Treponema pallidum immobilization or fluorescent treponemal antibody absorption test
11. positive ANA of abnormal titer in absence of drugs associated with "drug-induced lupus"

SLE in Pregnancy
Women with SLE have no increase in infertility
Outcome is best for mother and child when SLE has been controlled for at least 6 months prior to pregnancy
7-33% of women with SLE have flares during pregnancy

Pregnancy Complications with SLE
Preeclampsia
Fetal Loss
Preterm Delivery
Low Birth Weight Infant
Deep Vein Thrombosis/Pulmonary Embolism

Neonatal Lupus
Occurs in about 2% of babies born to mothers w/ anti-Ro/SSA and or anti-La/SSB antibodies
Caused by passage of the antibodies from the mother’s bloodstream across the placenta to the developing baby after about 20 weeks
Signs of neonatal lupus includes red, raised rash on the scalp and around the eyes that resolves by 6-8 months (because the antibodies clear the blood stream)
SLE complications in babies: complete heart block  and learning disabilities
Risk of neonatal lupus in subsequent pregnancy is 17%..

Infective peritonitis

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Primary--->the peritoneal infection is not directly related to other intra-abdominal abnormalities.
Secondary --->an intra-abdominal process, such as a ruptured appendix or a perforated peptic ulcer, is evident.
Tertiary ---> a later stage of the disease, when clinical peritonitis and signs of sepsis persist after treatment for secondary peritonitis, and no pathogens or only low-grade pathogens are isolated from the peritoneal exudate.

Primary peritonitis, sometimes referred to as spontaneous bacterial peritonitis (SBP): infection of the peritoneal cavity without an evident source.

Primary peritonitis may occur in children without predisposing disease
particularly in children with cirrhosis and in 2% of children with NS, (some reported in UTI)

Among 63 consecutive adult patients with cirrhosis and ascites studied prospectively using optimal aerobic and anaerobic bacteriologic techniques, primary peritonitis was found in 5.

Bacteriologic Characteristics
Several decades ago, the organisms reported to cause primary peritonitis in children were Streptococcus pneumoniae and group A streptococci.
By the 1970s the number of nephrotic children with streptococcal peritonitis had declined.
The relative frequency of peritonitis caused by gram-negative enteric bacilli had increased.
In cirrhotic patients, microorganisms presumably of enteric origin account for up to 69% of the pathogens.
E coli is the most frequently recovered pathogen, followed by Klebsiella pneumoniae, S. pneumoniae, and other streptococcal species, including enterococci.
Anaerobes and microaerophilic organisms are infrequently reported. 
In one series, sterile cultures occurred in 35% of patients with clinical findings consistent with primary peritonitis.

The WBC in peritoneal fluid usually is greater than 300 cells/mm3 (in 85% of cases, >1000/mm3), with PMN predominating in > 80% of cases.

Ascitic fluid pH < 7.35 and a lactate > 25 mg/dl were more specific but less sensitive than a WBC> 500 cells/mm3
using all three parameters together increased the diagnostic accuracy.
Gram staining of the sediment, when positive, is diagnostic, but it is negative in 60 to 80% of patients with cirrhosis and ascites.

Diagnosis
One of exclusion of a primary intra-abdominal source of infection.
Oral and intravenous contrast with CT scanning has greatly enhanced detection of intra-abdominal sources of peritonitis.
Patients with primary peritonitis usually respond within 48 to 72 hours to appropriate antimicrobial therapy.
An exponential rate of decline in the number of ascitic fluid leukocytes after the initiation of antimicrobial therapy for primary peritonitis  differentiate primary from secondary bacterial peritonitis.
Paracentesis for smear and culture is indicated in all cirrhotic patients with ascites and in children with gross proteinuria and abdominal pain.
However, paracentesis is not without hazard.
Major complications include perforation of the bowel with generalized peritonitis or abdominal wall abscess and serious hemorrhage.

Cardiomyopathy in neonates and children

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Some cardiomyopathies are treatable
Cardiomyopathy may presents as recurrent wheeze

Classification of Cardiomyopathy
Dilated
Chronic
Acute Viral myocarditis (Inflammatory Cardiomyopathy)
Hypertrophic
Restrictive

Dilated Cardiomyopathy
Insidious onset, may be acute in up to 25% of patients, exacerbated by a complicating LRTI
Cough, poor feeding, irritability, and shortness of breath are usually the initial presenting symptoms.
Pallor, sweating, easy fatigability, failure to gain weight, and decreased urine output may be present.
Wheezing may be an important clinical sign, suggesting congestive heart failure (CHF) manifestation in infants.
Chest pain, palpitations, orthopnea, hemoptysis, frothy sputum, sudden death, abdominal pain, syncope, and neurologic deficit are other modes of presentation (20%).
Cardiomegaly detected incidentally on a chest radiograph or an arrhythmia detected incidentally on an ECG may be the basis for initial cardiac referral.
Approximately 50% of patients with dilated cardiomyopathy (DCM) have a history of preceding viral illness. A detailed family history for familial cardiomyopathy is revealing in up to 25% of cases.

In established disease, features of CCF are dominant.
Major cardiac findings include cardiomegaly, quiet precordium, tachycardia, gallop rhythm (S3 and/or S4), accentuated P-2, and murmurs of mitral and tricuspid regurgitation. Murmurs may be inconspicuous initially when presenting in acute heart failure.
Infants often present with predominantly respiratory signs and, in the absence of a precordial heave or prominent murmur, the underlying cardiac disease may remain undiagnosed until cardiomegaly is detected on chest radiograph.

ECG
Presence of Q waves and inversion of T waves in leads I, II, aVL, and V4 through V6 (anterolateral infarction pattern): ALCAPA
Significant arrhythmia: Arrythmia causing DCM
Low Voltage complexes: Pericardial effusion

ECHO
Dilated left ventricle (>95th percentile) with global hypokinesia (fractional shortening<25%, ejection fraction <;50%), and no demonstrable structural heart disease: DCM Left ventricular posterior wall hypokinesia with hyper-echoic papillary muscles, retrograde continuous flow into proximal pulmonary artery: ALCAPA Significant pericardial effusion with satisfactory left ventricular ejection fraction: Pericardial effusion...

Lower Extremity Vascular Disease

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Pathophysiology
Most predominant cause is atherosclerotic disease
Other causes include antiphospholipid syndrome, popliteal aneurysms, adventitial cystic disease, popliteal artery entrapment, and trauma.
Collateral circulation allows for blood flow to all areas of the lower extremity in the face of localized occlusive disease
Muscle arterial resistance can be decreased to allow a large increase in blood flow. This is physiologic during exercise and compensatory during ischemia
As occlusive disease progresses, it usually involves multiple sites in the lower extremity vasculature
The first symptoms are noted by the patient during exercise because the leg is no longer able to increase blood delivery in the normal fashion
Claudication, is reproducible lower extremity muscle pain on walking that is relieved by rest
Most commonly, it involves the calf.
As ischemia progresses, pain is encountered at rest.
With critical ischemia, the patient experiences rest pain and wounds are unable to heal, so that the patient is predisposed to infection, gangrene, and limb loss
Rest pain initially begins in the forefoot (metatarsalgia) and toes and progresses proximally.
Patients often notice a beneficial effect of gravity on their arterial blood flow.
Many let their legs hang over the side of the bed in a dependent fashion to increase the effect of gravity, which augments minimal perfusion and decreases pain.
Conversely, symptoms of rest pain are provoked and worsened when the extremity is elevated...

Non-invasive Techniques
Ankle-Brachial Index
Useful in predicting the likelihood of wound healing
Amputations healed in all patients with an ABI above 70%
Healing did not occur in 25% of those with an ABI below 70%
Simple and inexpensive
In diabetics  is often unreliable because of abnormal wall calcification and noncompressibility
Additional information can be obtained by measuring pressures at various levels of the lower extremity
Gradients of more than 20 mm Hg are diagnostic of a hemodynamically significant lesion
Duplex Ultrasound
Exercise stress test can be performed...

Update on motor neuron diseases

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Upper motor neurons (UMN) are responsible for conveying impulses for voluntary motor activity
UMN send fibers to the LMN, and that exert direct or indirect supranuclear control over the LMN.
Lower motor neurons (LMN) directly innervate the skeletal muscle

Motor cortex: the UMNs are located in the primary motor cortex, Brodmann’s area 4, and the premotor areas, Brodmann’s area 6 (secondary motor complex and premotor complex).
Betz’s giant pyramidal neurons are the distinct group of neurons in layer 5 and other smaller neurons initiate the contraction of the small groups of the skeletal muscles and control the force and contraction. 

Signs and Symptoms of UMN Disorders
Loss of dexterity, voluntary skillful movements. It may be expressed as stiffness, slowness, and clumsiness, in particular, rapid repetitive motions.
weakness is mild. UMN: UEx extensors, and LEx flexors.
Spasticity is hallmark of the UMN disease. Spasticity is a state of sustained increase in muscle tension in response to muscle lengthening, in particular, with passive movements.
Pathological hyperreflexia.
Pseudobulbar palsy is hallmark of the UMN disorder, which is characterized by sudden unmotivated crying or laughing.

The LMNs are located in the brainstem and spinal cord
The spinal LMNs are also known as anterior horn cell. The neurons are clustered in nuclei, forming longitudinal columns.
Dorsal anterior horn cells innervate distal muscles, ventral located cells- proximal muscles, medially located neurons- truncal and axial muscles. Markedly enlarged lateral parts of the cervical and lumbar (lower thoracic) anterior horns innervate arm, hand, and leg muscles.
Large spinal cord LMNs are called alpha neurons.

Signs and Symptoms of Lower Motor Neuron Dysfunction
Weakness: denervation as well as decreased number of functional LMN units reduces overall muscles strength.
Muscle atrophy and Hyporeflexia
Muscle hypotonicity and flaccidity
Fasciculations
Muscle cramps

UMN DISORDERS
Primary Lateral sclerosis: a diagnosis of exclusion
Hereditary spastic paraplegia: AD disorder
HTLV-1 associated myelopathy: X-linked recessive inheritance,  increased serum of very-long-chain fatty acids
Adrenomyeloneuropathy
Lathyrism: history of consumption of chickpeas

Disorders of LMNs
Poliomyelitis
Multifocal Motor Neuropathy
Benign Focal Amyotrophy
Hopkins’ syndrome: Acute post-asthmatic amyotrophy
SMA
Bulbo-Spinal Muscular Atrophy (BSMA; Kennedy's Syndrome; X-linked)
Primary Muscular Atrophy (PMA)..

Rheumatic Fever

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Etiology
Acute rheumatic fever is a systemic disease of childhood,often recurrent that follows group A beta hemolytic streptococcal infection
It is a delayed non-suppurative sequelae to URTI with GABH streptococci.
It is a diffuse inflammatory disease of connective tissue,primarily involving heart,blood vessels,joints, subcut.tissue and CNS

Clinical Features
1.Arthritis
Migratory polyarthritis, involving major joints
Commonly involved joints-knee,ankle,elbow & wrist
Occur in 80%,involved joints are exquisitely tender
In children below 5 yrs arthritis usually mild but carditis more prominent
Arthritis do not progress to chronic disease

2.Carditis
Manifest as pancarditis(endocarditis, myocarditis and pericarditis),occur in  40-50% of cases
Carditis is the only manifestation of rheumatic fever that leaves a sequelae & permanent damage to the organ
Valvulitis occur in acute phase
Chronic phase- fibrosis,calcification & stenosis of heart valves.

3.Sydenham Chorea
Occur in 5-10% of cases
Mainly in girls of 1-15 yrs age
May appear even 6 months after the attack of rheumatic fever
Clinically manifest as-clumsiness, deterioration of handwriting,emotional lability or grimacing of face

4.Erythema Marginatum
Occur in <5%.
Unique, transient lesions of 1-2 inches in size
Pale center with red irregular margin
More on trunks & limbs & non-itchy
Worsens with application of heat
Often associated with chronic carditis

5.Subcutaneous nodules
Occur in 10%
Painless,pea-sized,palpable nodules
Mainly over extensor surfaces of joints,spine,scapulae & scalp
Associated with strong seropositivity
Always associated with severe carditis...

Objectives Review the indications for first trimester ultrasound Discuss utilization of ultrasound Review measurements and how they apply to dating criteria Discuss how to document an ultrasound in the medical record

Indications (1 st Trimester) Dating of pregnancy Size vs dates discrepancy; multiple gestation determination * (1 st Trimester)* Vaginal bleeding Abdominal or pelvic pain: rule out ectopic pregnancy/ torsion/ heterotopic pregnancy/ ovarian cyst ***Not credentialed to do*** To confirm viability

Pregnancy Dating with 1 st trimester ultrasound The only utility for “routine” ultrasound as determined by the RADIUS study Early dating is the most accurate (+/- 5-7d or 8%) Better defines timing for later testing and interventions Triple/Quad test Tocolysis/Steroids Reduces the incidence of induction for postdates

Measurements Mean Sac Diameter Should be measured in 3 dimensions May be all that is visible at the discriminatory zone; IUP best confirmed with some fetal element, such as a yolk sac

The Early Gestational Sac
Measurements Embryonic Crown-Rump Length (CRL) Measurement of a CRL with fetal cardiac activity is the best measurement for dating purposes Accurate through the 12 th week of gestation

Late 1 st Trimester—10 week
Typical Measurements There are tables for determining gestational age based on: Gestational Sac Measurement Crown-Rump Length All of the U/S machines at NHP contain software which perform these calculations. The measurements will trigger the gestational age determination.

Early Pregnancy Failure Failure of appropriate interval growth by US of embryo Fetal pole/yolk sac should be seen by the time the MSD is 20 mm (not as accurate as FCA though) Fetal Cardiac Activity should be seen by the time the CRL is 4mm (5mm per AIUM) If not, may repeat the u/s in one week

Rule out ectopic Classic triad—amenorrhea, vaginal bleeding, pain Must have a high index of suspicion Even more so in the face of risk factors Three primary tools for evaluation Physical exam Quantitative β HCG Ultrasound

Lab and Ultrasound Discriminatory Zone—the quant β -hCG level at which one would expect to be able to identify an intrauterine pregnancy For vaginal sonography—1200-1500 (1000-2000 per ACOG) For abdominal sonography—3000-4000 If the quant β -hCG is at or above the discriminatory zone, AND no IUP can be identified, the pregnancy may be ectopic

Background to Guidelines Mortality rates from intrahepatic cholangiocarcinoma have steeply risen over the course of the last 30y and continue to rise 1998+9 = 1000 deaths / year Men = Women Previously no clear national consensus for optimal diagnosis and treatment

Risk Factors Age (65% are >65y) PSC (lifetime risk = 5-15%) Chronic intraductal gall stones Bile duct adenoma + biliary papillomatosis Caroli’s disease (cystic dilatation of ducts) Lifetime risk = 7% Choledochal cysts (5% will transform with time) Smoking Chemical Exposure ( Thorotrast, aircraft, rubber) Tropiocal (liver flukes, chronic typhoid carriers)

Anatomical Classification A) Intrahepatic (20-25%) B) Perihilar (50-60%) “Klatskin” = involve the duct bifurcation Many are coded as intrahepatic C) Distal Extrahepatic (20-25%) D) Multifocal (5%)
Bismuth’s Perihilar Classification Type 1 Below the confluence Type 2 Involving the confluence but not the L or R duct Type 3 Occluding the CHD and involving either the L (IIIa) or the R (IIIb) hepatic duct Type 4 Multicentric or Involve the CHD + both the L and the R hepatic ducts

Clinical Features Obstructive Jaundice RUQ pain, Fever + Rigors Suggesting cholangitis Systemic (malaise, weight loss, fatigue) Deranged LFTs Usually present late (esp. prox tumours)

Treatment – Curative Surgery 5y Survival for intrahepatic Ca = 9-18% 5y Survival for proximal Ca = 9-18% 5y Survival for distal Ca = 20-30% Survival depends on stage with tumour free margins absence of LN involvement Median Survival With hilar involvement = 12-24/12 Without hilar involvement = 18-30/12

Palliative Procedures Stenting Reduces sepsis Improves survival Surgical bypass has not proved superior Irradiation Intraoperative Coeliac plexus block

Resection Reporting 1) Tumour Type Extent Blood / lymphatic involvement Perineural invasion (worse prognosis) 2) Margins 3) Regional LNs (peripancreatic = distant) 4) Additional pathological findings (PSC) 5) Metastases

Decompression Pre-op biliary drainage / stenting is not advised if resection being considered May be necessary in severely malnourished or in acute suppurative cholangitis Preop placement of biliary catheters may be a helpful technical aid when dissecting a proximal Ca

Stenting Complex CholangioCa MRCP will help planning management ? Bilateral > unilateral Plastic Vs Metal Metal stents in those due to survive >6/12 Metal = shorter hospital stay Stenosis of metal stents can be treated with Cotton-Leung plastic stent through lumen Mesh metal stent Semicovered stents (?reduce Ca ingrowth)

Pyogenic Hepatic Abscesses

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Etiology
Biliary disease accounts for 21-30%, with extrahepatic obstruction leading to ascending cholangitis and abscess. Also CBD stones, benign and malignant tumors, biliary enteric anastamoses.
Infection via portal system Infectious process originates in abdomen, reaches liver by embolization of portal system. Appendicitis, diverticulitis, IBD, proctitis
Hematogenous. Via hepatic artery. From systemic septicemia. No cause in 50% of cases, but increased in diabetics and metastatic cancer.

Pathophysiology:
Access to liver by direct extension from nearby organs. Through portal vein and hepatic artery. Hepatic clearance of bacteria via portal system is a normal phenomena, but organism proliferation, tissue invasion and abscess can occur with biliary obstruction, poor perfusion, microembolization.

Microbiology:
Most contain more than one organism, with source biliary or enteric. Blood cultures positive in 33-65%. E.Coli 33%. Klebsiella 18%. Bacteroides 24%. Streptococcal 37%.

Clinical:
Fever, right upper quadrant pain (80%). Right shoulder pain, pleuritic chest pain. Fever 87-100%. Anorexia, weight loss, mental confusion. Physical exam shows RUQ tenderness, hepatomegaly, liver mass, jaundice.

Indications For Open Drainage:
Abscess not amenable to percutaneous drainage Co-existing intra-abdominal disease that requires operative management. Failure of antibiotic therapy. Failure of percutaneous aspiration or drainage.

Relative Contraindications:
Age older than 70. Multiple abscesses. Polymicrobial infection. Presence of associated malignancy or immunosupressive disease. Multiple medical problems

Percutaneous Drainage CT or US guided placement of a catheter. Drain is removed once abscess cavity collapses. Success 80-87%. Consider open drainage if fails, or patient worsens over 72 hrs.
Complications of Percutaneous Drainage Perforation of a viscous. Pneumothorax. Bleeding. Leakage of pus into the abdomen. Immunocompromised patients with multiple abscesses are best treated with high dose antibiotics rather than open or percutaneous drainage.
Surgical Therapy Five indications as previously discussed. Presence of peritoneal signs mandates emergent exploration. Transthoracic, extraperitoneal, transperitoneal. Transperitoneal is preferred as intra-abdominal pathology can be dealt with.
Complications Result from rupture of abscess into adjacent organs or cavities. These include both pleuropulmonary and intrabdominal types. Pleuropulmonary are themost common 15-20%, include effusions, empyema, bronch-hepatic fistula. Intraabdominal include subphrenic abscess, rupture into peritoneal cavity, stomach, colon, vena cava, or kidney.

Orbital Trauma

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Case Presentation 12 hrs s/p blepharoplasty – c/c: bleeding eyelid. “I’ll only see a plastic surgeon.” PE- venous blood from incision VSS, eye grossly normal VA – 20/20 bilaterally , PERL Plastics: “What kind of insurance does he have? Cash? I’ll be down.” 3- 4 hours later- repeat PE: VSS, right eye dilates to light.

Blowout Fracture- Presentation Definition Symptoms Pain Double vision Numbness to cheek tenderness Critical signs Restricted EOM Subcutaneous emphysema Globe displacement Globe trauma 32%
Etiology:
Blowout Fracture - Etiology Theories Waterhouse 1999 Buckling Hydraulic Fracture site Inferior wall Medial wall Superior rim CNS injury CSF leak Intracranial - bleed
Blowout Fracture- X-ray Screening Teardrop sign
Blowout fracture- Management Consults Nasal Decongestants Antibiotics Evidence? Sneezing/Blowing Nose Disposition With entrapment Without entrapment Associated injuries

Ruptured Globe – Presentation Incidence 1.1-3.5% Symptoms Predictive signs 1) VA showing light perception or worse. 2) Abnormal deep/shallow anterior chamber. 3) Opacity preventing view of fundus. 4) IOP of 5 or less.
Ruptured Globe - Management Diagnosis Suspected – STOP Examination Do NOT put pressure on globe RSI Br. J of Anesth 1999 Antibiotics Tetanus Antiemetic CT scan Prepare for surgery.

Retrobulbar Hemorrhage - Presentation Definition Symptoms Critical signs Proptosis Visual acuity Marcus-Gunn pupil Red desaturation
Management “TIME IS RETINA” Progressive Lateral canthotomy CT scan of orbit Disposition

Hyphema- Presentation Definition Symptoms Grading 0 RBC’s I <1/3 II 1/3 – 1/2 III >1/2 IV eight ball
Hyphema- Management Ophthalmic consult Pupillary play/Eye Patch Reverse Trendelenburg Anesthesia /Anti-emetic IOP control > 30 mmHg (>24 mmHg in HbSS) Admission HbSS Anti-coagulated > Grade I Decreasing VA ED evaluation >1 day after initial injury. Complications Re-bleed Post-traumatic glaucoma

Tropical Infections in ICU

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Case Presentation:32-year male PC: fever x 7 days, jaundice x 3 days, confusion x 1 day Exam: Temp - 105 0 F; PR 128/min; RR 24/min; BP 90/70 mm Hg; icteric; drowsy, confused & disoriented; hepatomegaly present

Acute Undifferentiated Febrile Illness:Acute -- <14 days Undifferentiated -- initial symptoms and signs non-contributory Fever -- oral temperature ≥101 0 F

Differential Diagnosis:Malaria ( P falciparum ),Scrub typhus, Leptospirosis, Dengue fever

Malaria:
Pathophysiology:
Mechanical microcirculatory obstruction Caused by cytoadherence to the vascular endothelium of parasitized RBC  sequestration & obstruction of small vessels Intra-vascular hemolysis

Clinical Features:
Severe Malaria:
Severe Malaria Cerebral malaria (unarousable coma not attributable to any other cause in a patient with falciparum malaria) Severe normocytic anemia (< 5 gm/dl) Hypoglycemia Metabolic acidosis Acute renal failure (S. creatinine > 3 mg/dl) ARDS Shock ("algid malaria") DIC Hemoglobinuria Hyperparasitemia (>5%)

Parasitological Diagnosis:
Microscopy Rapid diagnostic tests QBC Antigen detection

Diagnosis:
Microscopy:Low cost High sensitivity & specificity Species identification Quantification
Quantitative Buffy Coat (QBC) Test:Staining of the centrifuged & compressed red cell layer with acridine orange & examining under UV light source Comparison with peripheral smear: Faster More sensitive Species identification possible Specialized equipment & consumables Expensive
Rapid Tests: Immunochromatographic tests Capture of the parasite antigens from the peripheral blood using either monoclonal or polyclonal antibodies Histidine-rich protein 2 of P. falciparum Pan-malarial Plasmodium aldolase Parasite specific LDH

Scrub Typhus:
Etiology: O tsutsugamushi Three major serotypes - Karp, Gilliam & Kato Vector: chiggers (larva of trombiculid mite) Reservoir: chiggers & rats Transovarian transmission Normal cycle: rat to mite to rat Humans are accidentally infected

Pathophysiology No known toxins Destruction of cells Endothelial injury Lympho-histiocytic vasculitis

Clinical Features:
Incubation period: 1 to 3 weeks Sudden onset of fever, headache & myalgia Delirium, nausea, vomiting, cough, jaundice Maculopapular rash Begins on trunk and spreads to extremities (centrifugal spread) Eschar

Complications:
Hepatitis ,Aseptic meningitis / meningoencephalitis ,Thrombocytopenia ,ARDS / Pneumonitis ,Renal failure ,Shock ,Fetal loss

When should scrub typhus be suspected?:
Undifferentiated febrile illness with: Pathognomonic eschar Evidence of multisystem involvement, especially with: - Transaminase elevation - Thrombocytopenia - Leukocytosis

Lab Diagnosis:
Serology Weil-Felix: poor sensitivity & specificity IFA: ‘gold standard’ ELISA for Ig G & Ig M antibodies (recombinant 56 kd antigen): sensitivity & specificity >90%

eptospirosis:
Etiology: L interrogans Most widespread zoonosis in the world Peak incidence during rainy season Occupational & recreational exposures Source of infection in humans: direct or indirect contact with the urine of an infected animal Portal of entry: abrasions or cuts on skin, conjunctiva

Clinical Features:
Biphasic clinical presentation Acute or bacteremic phase lasting ~1 week Immune phase, characterized by antibody production and leptospiruria Anicteric leptospirosis Abrupt onset of fever, chills, headache, myalgia, abdominal pain, conjunctival suffusion , transient skin rash Icteric leptospirosis (Weil’s disease) Occurs in 5-15% of patients Jaundice Proteinuria, hematuria, oliguria and/or anuria Pulmonary hemorrhages, ARDS Myocarditis

Diagnosis:
CPK levels Culture (blood, CSF, urine) Positive serology Microscopic Agglutination Test (MAT) (using a range of Leptospira strains for antigens that should be representative of local strains) IgM ELISA..

Arrhythmias associated with:
cardiac arrest
acute coronary syndromes
chronic CAD / LV dysfunction
coronary artery bypass surgery

Arrhythmias associated with ACS
Routine use of anti-arrhythmic drugs is not recommended following MI.

Patients who have suffered a recent myocardial infarction and with LVEF ≤ 0.40 and either diabetes or clinical signs of heart failure should receive eplerenone unless contraindicated by the presence of renal impairment or high potassium levels.

Arrhythmias associated with chronic CHD / decreased LVEF
ATRIAL FIBRILLATION
Choice of antiarrhythmic drug
Rate vs rhythm control
Non-pharmacological therapies

Arrhythmias associated with chronic CHD/decreased LVEF
AF-Rate control
Rate control is the recommended strategy for management of patients with well tolerated atrial fibrillation.
 Ventricular rate in AF should be controlled with beta blockers, rate-limiting calcium channel blockers (verapamil or diltiazem), or digoxin.
 Digoxin does not control rate effectively during exercise and should be used as first line therapy only in people who are sedentary, or in overt heart failure.
Patients with AF who remain symptomatic despite adequate rate control should be considered for rhythm control.

AF-Rhythm control
Amiodarone or sotalol treatment should be considered where prevention of atrial fibrillation recurrence is required on symptomatic grounds.
 Patients with atrial fibrillation who are severely symptomatic despite optimum tolerated medical therapy should be referred to a cardiac rhythm specialist for consideration of non-pharmacological therapy, e.g. radiofrequency ablation.

VENTRICULAR ARRHYTHMIAS
Implantable Cardioverter Defibrillators in primary and secondary prevention
Antiarrhythmic drug therapy

Patients with moderate to severe LV dysfunction (e.g. ejection fraction <0.35), in NHYA Class I-III at least one month after myocardial infarction should be considered for ICD therapy.
 Patients with spontaneous non-sustained ventricular tachycardia (especially if sustained ventricular tachycardia is inducible), severely impaired ejection fraction (<0.25) or prolonged QRS complex duration (>120ms) should be prioritised for ICD implantation.
 Patients meeting criteria for ICD implantation who have prolonged QRS duration (>120ms) and NYHA class III-IV symptoms should be considered for CRT-D therapy...

What Is Juvenile Rheumatoid Arthritis?

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What Is Juvenile Rheumatoid Arthritis?:
Arthritis is a disease in a person’s joints that cause swelling and pain where the bones meet each other, resulting in stiffness and loss of motion Juvenile Rheumatoid Arthritis is arthritis in children under 16 years old with inflammation lasting at least 6 weeks.Juvenile rheumatoid arthritis is different from adult rheumatoid arthritis Kids have different symptoms The damage to bones is different

How Is Juvenile Rheumatoid Arthritis Different From Adult Rheumatoid Arthritis?:
Main Difference: Many people with JRA outgrow the illness, while adults usually have lifelong symptoms. Studies estimate that by adulthood, JRA symptoms disappear in more than half of all affected children. Unlike rheumatoid arthritis in an adult, JRA may affect bone development as well as the child's growth.

Who Gets JRA?:
About 1 child in every 1,000 develops some type of juvenile arthritis. Approximately 75,000 children in the U.S. Can affect children at any age, but uncommon in the first six months of life

Why Do Kids Get JRA?:
Cause is unknown Research suggests a genetic predisposition Triggered by an environmental factor, such as a virus JRA is an autoimmune disease Immune system mistakes healthy cells for harmful ones. Body releases chemicals to fight healthy cells causing pain and swelling.

Types of Juvenile Rheumatoid Arthritis:
There are three types JRA. Pauciarticular: fewer than five joints are affected. Usually knees and large joints. Polyarticular: affects five or more joints. Joints on both sides of body are affected. Smaller joints like hands or toes. Systemic JRA: affects many parts of the body. Heart, lungs and liver could be affected as well.

Signs/symptoms:
Signs/symptoms Limping Stiffness when awakening Reluctance to use an arm or leg Reduced activity level Persistent fever Joint swelling

Pathophysiology:
Pathophysiology Chronic inflammation of synovium is characterized by B lymphocyte infiltration and expansion. Macrophages and T-cell invasion are associated with the release of cytokines, which evoke synoviocyte proliferation.2001 study by Scola et al : Found synovium to contain m-RNA for vascular endothelial growth factor, angiopoietin 1, and their respective receptors This suggests that induction of angiogenesis by products of lymphocytic infiltration may be involved in persistence of disease. The resulting thickened pannus causes joint destruction. In many patients, predominance of cytokines associated with tissue destruction, including interleukin-6 and TNF, suggests the possibility of improved responsiveness to specific biologic agents targeting these factors.

How Is JRA Diagnosed?:
Complete health history Physical examination to look for joint inflammation, rashes, nodules, signs of internal organ inflammation and/or eye problems Laboratory tests to help rule out other diseases Erythrocyte sedimentation rate Hemoglobin and blood count testing Urinalysis X-rays Tests of joint, blood and tissue fluids to check for infections or inflammation

Treatment Options:
Control symptoms, prevent joint damage, and maintain function 1. Non-steroidal Anti-Inflammatory Drugs (NSAIDS) Motrin or Advil 2. Disease Modifying Drugs (DMARDS) Hydroxychloroquine: Plaquenil Sulfasalazine: Azulfidine Methotrexate: Rheumatrex

Respiratory Acidosis
Respiratory acidosis is defined as a pH less than 7.35 with a PaCO2 greater than 45 mm Hg.
Acidosis is caused by an accumulation of CO2 which combines with water in the body to
produce carbonic acid, thus, lowering the pH of the blood. Any condition that results in
hypoventilation can cause respiratory acidosis. These conditions include:
• Central nervous system depression related to head injury
• Central nervous system depression related to medications such as narcotics, sedatives, or
anesthesia
• Impaired respiratory muscle function related to spinal cord injury, neuromuscular diseases,
or neuromuscular blocking drugs
• Pulmonary disorders such as atelectasis, pneumonia, pneumothorax, pulmonary edema, or
bronchial obstruction
• Massive pulmonary embolus
• Hypoventilation due to pain, chest wall injury/deformity, or abdominal distension

Respiratory Alkalosis
Respiratory alkalosis is defined as a pH greater than 7.45 with a PaCO2 less than 35 mm Hg.
Any condition that causes hyperventilation can result in respiratory alkalosis. These conditions
include:
• Psychological responses, such as anxiety or fear
• Pain
• Increased metabolic demands, such as fever, sepsis, pregnancy, or thyrotoxicosis
• Medications, such as respiratory stimulants.
• Central nervous system lesions

Metabolic Acidosis
Metabolic acidosis is defined as a bicarbonate level of less than 22 mEq/L with a pH of less
than 7.35. Metabolic acidosis is caused by either a deficit of base in the bloodstream or an
excess of acids, other than CO2. Diarrhea and intestinal fistulas may cause decreased levels of
base. Causes of increased acids include:
• Renal failure
• Diabetic ketoacidosis
• Anaerobic metabolism
• Starvation
• Salicylate intoxication

Metabolic Alkalosis
Metabolic alkalosis is defined as a bicarbonate level greater than 26 mEq/liter with a pH greater
than 7.45. Either an excess of base or a loss of acid within the body can cause metabolic
alkalosis. Excess base occurs from ingestion of antacids, excess use of bicarbonate, or use of
lactate in dialysis. Loss of acids can occur secondary to protracted vomiting, gastric suction,
hypochloremia, excess administration of diuretics, or high levels of aldosterone.

Restrictive Lung Diseases

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Chronic Restrictive Lung Diseases
Group of different diseases
Similar clinical, pulmonary function test and pathological findings
Represent 15% of non-infectious diseases of lungs
End-stage: diffuse interstitial pulmonary fibrosis (Honeycomb lung)

Primary lung disease
Acute: Acute Respiratory Distress Syndrome ARDS
Chronic:
Occupational: Asbestosis, silicosis, coal worker pneumoconiosis
Interstitial lung disease (interstitial pneumonia), Idiopathic pulmonary fibrosis
Immune diseases: Sarcoidosis, SLE, RA, Wegener
Physical injury: : Radiation
Drugs: Chemotherapy, methotrexate

Idiopathic Pulmonary Fibrosis
Cryptogenic fibrosing alveolitis
Unknown etiology
Diffuse interstitial fibrosis
Sever hypoxemia, and cyanosis
Male>Female, 60y
Diagnosis of exclusion

Pathogenesis:
Alveolar wall injury
Alveolitis: inflammation, edema
Neutrophil, macrophages, lymphocytes
Interstitial Fibrosis
? Immune disorder: association with immune diseases: RA, SLE, Sjogren….
Macrophages: IL-8, FGF, TGF-beta, PDGF

Sarcoidosis
Multisystem disease
Unknown etiology
Non-caseating granuloma in many tissues and organs
Diagnosis of exclusion

Presenting Picture:
Bilateral hilar lymphadenopathy
Lung involvement, lung nodules
Other organs: skin, eye, any tissue
Adult, younger than <40y
Common in US blacks
Higher in non-smokers..

Traumatic Brain Injury

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Traumatic Brain Injury (TBI) Definition: A nondegenerative, noncongenital insult to the brain from an external mechanical force, possibly leading to permanent or temporary impairments of cognitive, physical, and psychosocial functions with an associated diminished or altered state of consciousness.

Mechanism of Injury
MVAs are the leading cause of TBI in the United States and account for approximately 50% of all TBIs. These include automobiles, motorcycles, bicycles and pedestrian struck.  MVAs are also the leading cause of TBIs in individuals under the age of 75.

Falls are the 2nd leading cause of TBI, accounting for 20-30% of all TBIs. In individuals aged 75 years and older, falls are the most common cause of TBI.

Firearms are the 3rd leading cause of TBI (12% of all TBIs).

Sports, Recreation, Physical Violence (eg. child abuse)

Alcohol is a major factor in many TBIs and often is associated with the leading causes of TBI.

Classification
Closed Head Injury: Occurs when the head forcefully collides with another object (for example the windshield of a car) but doesn't fracture or penetrate the skull.

Open Head Injury: Occurs when an object (for example a bullet) fractures the skull and debris enter the brain.

Focal: Confined to one area of the brain. 
Diffuse: Involving more than one area of the brain.

Focal injury
Associated with:
Contusion: bruising of brain
Intracranial hemorrhage (hematoma): heavy bleeding in the skull. Hemorrhage, due to rupture of a blood vessel in the head, can be extra-axial, meaning it occurs within the skull but outside of the brain, or intra-axial, occurring within the brain.
Extra-axial hemorrhages: subdural hematoma, epidural hematoma, and subarachnoid hemorrhage.
Intra-axial bleeds: intraparenchymal hemorrhage which occurs within the brain tissue itself and intraventricular hemorrhage which occurs into the ventricular system.

Diffuse 
Associated with:
Concussion: a shaking of the brain in response to sudden motion of the head
Diffuse axonal injury (DAI): extensive generalized damage to the white matter tracts of the brain and a major cause of unconsciousness after head trauma. 90% of patients with severe DAI never regain consciousness.
Coma: profound state of unconsciousness...

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