Blood

BLOOD

CIRCULATORY SYSTEM
* BLOOD
* HEART
* BLOOD VESSELS

FUNCTIONS OF BLOOD
* TRANSPORT
* PROTECTION
* REGULATION

TRANSPORT
* OXYGEN (O2)
* CARBON DIOXIDE (CO2)
* NUTRIENTS
* WASTES
* HORMONES
PROTECTION
* IMMUNE SYSTEM
o WHITE BLOOD CELLS
o ANTIBODIES
* CLOTTING SYSTEM
o PLATELETS
o FIBRINOGEN / FIBRIN

REGULATION
* BODY TEMPERATURE
* pH
* WATER BALANCE
* ELECTROLYTE BALANCE

BLOOD COMPOSITION
BLOOD IS COMPRISED OF TWO MAIN COMPONENTS:
* PLASMA
* FORMED ELEMENTS
THESE COMPONENTS CAN BE SEPARATED BY CENTRIFUGATION
THE FRACTION OF THE BLOOD VOLUME COMPRISED OF RED BLOOD CELLS IS TERMED THE HEMATOCRIT

PLASMA COMPOSITION
* WATER (~90%)
* SOLUTES (~10%)
o PROTEINS (~8%)
o OTHER COMPOUNDS (~2%)
+ NUTRIENTS
+ GASES
+ WASTES
+ HORMONES
+ ELECTROLYTES

PLASMA PROTEINS
* MOST ABUNDANT PLASMA SOLUTE
* LIVER CAN PRODUCE 4 GRAMS OF PLASMA PROTEINS PER HOUR
* THREE MAJOR CATEGORIES
o ALBUMINS
o GLOBULINS
o FIBRINOGEN
ALBUMINS
* ~60% OF PLASMA PROTEINS
* SMALL
* TRANSPORT LIPIDS, HORMONES, CALCIUM, ETC.
* BUFFER BLOOD pH
* CONTRIBUTE TO VISCOSITY & OSMOLARITY
* INFLUENCE BLOOD PRESSURE, BLOOD FLOW, AND FLUID BALANCE

GLOBULINS
* ~36% OF PLASMA PROTEINS
* THREE SUBCLASSES
o ALPHA (a)
o BETA (b)
o GAMMA (g)
* ALPHA (a)
o VARIOUS FUNCTIONS, ESPECIALLY TRANSPORT
* BETA (b)
o VARIOUS FUNCTIONS, ESPECIALLY TRANSPORT
* GAMMA (g)
o COMPONENTS OF IMMUNE SYSTEM
o PRODUCED BY PLASMA CELLS, WHICH ARE DESCENDED FROM WHITE BLOOD CELLS

FIBRINOGEN
* ~4% OF PLASMA PROTEINS
* PRECURSOR OF FIBRIN
* INVOLVED IN BLOOD CLOTTING

PLASMA: NUTRIENTS
* SUGARS
* AMINO ACIDS
* FATS
* CHOLESTEROL
* PHOSPHOLIPIDS
* VITAMINS
* MINERALS

PLASMA: GASES
* OXYGEN (O2)
o REQUIRED FOR CELLULAR RESPIRATION
* CARBON DIOXIDE (CO2)
o PRODUCT OF CELLULAR RESPIRATION
* NITROGEN (N2)
o USUALLY PHYSIOLOGICALLY UNIMPORTANT
o WHY DO YOU THINK IT IS THERE?

PLASMA: WASTES
NITROGENOUS WASTES
* PRODUCTS OF CATABOLISM
o (ESP: AMINO ACID CATABOLISM)
* MOST ABUNDANT IS UREA
* REMOVED FROM BLOOD BY KIDNEYS
* EXCRETED THROUGH URINE
* RATE OF REMOVAL BALANCES RATE OF PRODUCTION

PLASMA: ELECTROLYTES
* SODIUM (Na+)
* CALCIUM (Ca2+)
* POTASSIUM (K+)
* MAGNESIUM (Mg2+)
* CHLORIDE (Cl-)
* BICARBONATE (HCO3-)
* PHOSPHATE (HPO42-)
* SULFATE (SO42-)
* VARIOUS IONS
* SODIUM IS THE MOST PREVALENT
* INCREASE BLOOD OSMOLARITY
o AFFECT BLOOD VOLUME
o AFFECT BLOOD PRESSURE

FORMED ELEMENTS
* ERYTHROCYTES (RED BLOOD CELLS)
* LEUKOCYTES (WHITE BLOOD CELLS)
* PLATELETS (CELL FRAGMENTS)

ERYTHROCYTE FUNCTIONS
* CARRY O2 FROM LUNGS TO CELLS
* CARRY CO2 FROM CELLS TO LUNGS
* HOW DO O2 AND CO2 RELATE TO THE FUNCTIONS OF A CELL?

ERYTHROCYTE QUANTITIES
* MEN: 4.6 – 6.2 MILLION/mL IN
o HEMATOCRIT 42 – 52 (% RBCs)
* WOMEN: 4.2 – 5.4 MILLION/mL
o HEMATOCRIT 37 – 48 (% RBCs)
* GENDER DIFFERENCES BASED ON:
o ANDROGENS INCREASE NUMBER
o MENSTRUAL LOSS DECREASES NUMBER
o BODY FAT (INVERSE RELATIONSHIP)
o FASTER CLOTTING IN MEN

ERYTHROCYTE STRUCTURE
* DISC SHAPED
* BICONCAVE
* 7.5 MICROMETER (mm) DIAMETER
* 2 MICROMETERS (mm) THICK

ERYTHROCYTE STRUCTURE
PLASMA MEMBRANE
* PHOSPHOLIPID BILAYER
* GLYCOPROTEINS, GLYCOLIPIDS
o DETERMINE BLOOD TYPE
* ACTIN AND SPECTRIN ON INNER SURFACE
o RESILIENCE / DURABILITY / PLIABILITY
* HIGH SURFACE AREA:VOLUME RATIO
o RESULT OF BICONCAVE SHAPE
o INCREASES RATE OF GAS DIFFUSION INTO AND OUT OF CELLS

ERYTHROCYTE STRUCTURE
CYTOPLASM
* LACKS ORGANELLES
o ESP: LACKS MITOCHONDRIA, NUCLEUS
o WHY IS THIS IMPORTANT?
o CANNOT REPAIR
o LIMITED LIFESPAN (~120 DAYS)
o CANNOT DIVIDE
o NEW CELLS FORMED IN BONE MARROW
* HEMOGLOBIN
o RED PIGMENT
o HIGH CONCENTRATION (33%)
o 280 MILLION MOLECULES PER CELL
o CARRIES MOST OF THE O2
o CARRIES SOME OF THE CO2
o PROTEIN & NON-PROTEIN COMPONENTS

HEMOGLOBIN
PROTEIN COMPONENT
* 4 POLYPEPTIDES (HETEROTETRAMER)
o 2 a-GLOBIN PROTEINS
o 2 b-GLOBIN PROTEINS
NON-PROTEIN COMPONENT
* 4 HEME GROUPS
o PORPHYRIN RING AND IRON ION
o IRON ION WITHIN HEME BINDS TO O2

ABO BLOOD TYPES
* DETERMINED BY SURFACE ANTIGENS
o GLYCOLIPIDS AND GLCOPROTEINS
+ (SUGARS ON CELL SURFACE)
o GENETICALLY DETERMINED
o RECOGNIZED BY ANTIBODIES
o INDIVIDUALS POSSESS ANTIBODIES TO ANTIGENS THEY THEMSELVES DO NOT POSSESS
o RECOGNITION OF THESE ANTIGENS BY ANTIBODIES CAUSES CELL CLUMPING
* DETERMINED BY GENE “I”
* THREE ALLELES
o IA
o IB
o i
* IA AND IB ARE CODOMINANT
* i IS RECESSIVE TO IA AND IB
* THREE ALLELES OF “I” GENE
* INDIVIDUALS POSSESS TWO COPIES
* FOUR BLOOD TYPES
o A GENOTYPE IAIA OR IAi
o B GENOTYPE IBIB OR IBi
o AB GENOTYPE IAIB
o O GENOTYPE ii

ANTIBODIES TO A AND B ANTIGENS
* APPEAR SHORTLY AFTER BIRTH
* PRESENT FOR ENTIRE LIFE
* PRODUCED IN RESPONSE TO SIMILAR ANTIGENS ON INTESTINAL BACTERIA
* CROSS-REACT WITH A AND B ANTIGENS
* TERMED “ANTI-A” AND “ANTI-B”
* CAUSE OF TRANSFUSION REACTIONS

Rh BLOOD TYPES
* DETERMINED BY SURFACE ANTIGENS
* UNRELATED TO ABO BLOOD TYPE
* GENETICALLY DETERMINED
* ALLELES OF THREE GENES
o C, c, D, d, E, e
o DD, Dd ARE Rh+
o dd MAY BE Rh-, DEPENDING ON ALLELES OF OTHER GENES
* ANTI-D ANTIBODIES NOT NORMALLY PRESENT
o PRESENT ONLY IN Rh- EXPOSED TO Rh+
o FIRST EXPOSURE NOT PROBLEMATIC
o SECOND EXPOSURE PROBLEMATIC
o TRANSFUSION / PREGNANCY
* IMMUNE RESPONSE PREVENTABLE
o RhoGAM (Rh IMMUNE GLOBULIN)

OTHER BLOOD GROUPS
* > 100 OTHER BLOOD GROUPS
* USEFUL IN GENETIC / BIOCHEMICAL TESTING
* RARELY CAUSE TRANSFUSION REACTIONS

ERYTHROCYTE DISORDERS
ANEMIA
* ERYTHROCYTE DEFICIENCY, OR
* HEMOGLOBIN DEFICIENCY
* THREE CLASSES
o INADEQUATE SYNTHESIS
o BLEEDING
o RBC DESTRUCTION
* CONSEQUENCES
o OXYGEN DEPRIVATION (HYPOXIA)
+ SHORTNESS OF BREATH
o REDUCED BLOOD OSMOLARITY
+ WATER RETENTION IN TISSUES (EDEMA)
o REDUCED BLOOD VISCOSITY
+ HEART BEATS FASTER
+ CARDIAC FAILURE
SICKLE-CELL ANEMIA
* ~0.25% OF AFRICAN AMERICANS
* GENETICALLY DETERMINED
* ABERRANT b-GLOBIN ALLELE (HbS)
o SINGLE AMINO ACID SUBSTITUTION
o GLUTAMIC ACID (HbA)  VALINE (HbS)
* CELLS SICKLE UNDER LOW OXYGEN
* MULTIPLE DELETERIOUS EFFECTS

* WHY IS THE FREQUENCY SO HIGH?
o MALARIA PREVALENT IN AFRICA
o Plasmodium PARASITE LIVES IN RBCs
o SURVIVES POORLY IN CELLS WITH HbS
o INDIVIDUALS WITH HbS LESS LIKELY TO DIE (HETEROZYGOTES MOST FIT)
o THUS, HbS PROVIDES PROTECTION

LEUKOCYTES
* 5,000 – 10,000 CELLS/mL
* FIVE TYPES:
o NEUTROPHILS 60 – 70 % 9 – 12 mM
o LYMPHOCYTES 25 – 33% 5 – 8 mM (most)
o MONOCYTES 3 – 8 % 12 – 15 mM
o EOSINOPHILS 2 – 4% 10 – 14 mM
o BASOPHILS <0.5 – 1% 8 – 10 mM
* GRANULOCYTES
o NEUTROPHILS
o EOSINOPHILS
o BASOPHILS
* AGRANULOCYTES
o LYMPHOCYTES
o MONOCYTES
LEUKOCYTES
NEUTROPHILS
* HIGHLY MOBILE
* INCREASE IN RESPONSE TO BACTERIAL INFECTIONS
* KILLS BACTERIA
o PHAGOCYTOSIS
o CHEMICALLY (BURST LYSOSOMES)

EOSINOPHILS
* INCREASE WITH ALLERGIES
* INCREASE WITH PARASITIC INFECTIONS
* PHAGOCYTOSIS
o ANTIGEN / ANTIBODY COMPLEXES
o ALLERGENS
* HYDROLYTIC ENZYME RELEASE
o RESPONSE TO HOOKWORM, TAPEWORM, ETC.
o TOO LARGE TO PHAGOCYTIZE
BASOPHILS
* GENERALLY NOT PHAGOCYTIC
* AID OTHER LEUKOCYTES
o RELEASE HISTAMINE
+ INCREASE BLOOD FLOW TO AREA
o RELEASE HEPARIN
+ INHIBIT CLOTTING
LYMPHOCYTES
* INCREASE IN IMMUNE RESPONSE
* SEVERAL SUBCLASSES
* VARIOUS IMMUNE FUNCTIONS
o ESP: SECRETE ANTIBODIES

MONOCYTES
* DIFFERENTIATE INTO MACROPHAGES
* PHAGOCYTOSIS OF PATHOGENS
* PHAGOCYTOSIS OF DEBRIS
* PRESENT ANTIGENS TO OTHER CELLS OF IMMUNE SYSTEM
PLATELETS
* 130,000 – 400,000 / mL
* NOT CELLS
o FRAGMENTS OF MEGAKARYOCYTES
o SMALL (2 – 4 mM DIAMETER)
* POSSESS VARIOUS ORGANELLES
* PSEUDOPODS
o AMOEBOID MOVEMENT
o PHAGOCYTOSIS
PLATELET FUNCTIONS
* SECRETE CLOTTING FACTORS
* SECRETE VASOCONSTRICTORS
* FORM TEMPORARY PLATELET PLUGS
* DISSOLVE OLD BLOOD CLOTS
* PHAGOCYTOSIS OF BACTERIA
* SECRETE CHEMICALS TO ATTRACT LEUKOCYTES TO SITES OF INFLAMMATION
* SECRETE GROWTH FACTORS

CONTROL OF BLEEDING
HEMOSTASIS
* VASCULAR SPASM
* PLATELET PLUG FORMATION
* COAGULATION
VASCULAR SPASM
* CONSTRICTION OF BROKEN VESSEL
* IMMEDIATE PROTECTION AGAINST BLEEDING
* MULTIPLE TRIGGERS
TRIGGERS OF VASCULAR SPASM
* PAIN RECEPTORS  NERVES  BLOOD VESSELS CONSTRICT
* SMOOTH MUSCLE OF BLOOD VESSELS CONSTRICT
* PLATELETS RELEASE SEROTONIN (CHEMICAL VASOCONSTRICTOR)
PLATELET PLUG FORMATION
* BLOOD VESSEL BROKEN
* COLLAGEN FIBERS EXPOSED
* PLATELETS BIND TO COLLAGE FIBERS
o FORM PSEUDOPODS
o ATTACH TO VESSEL AND OTHER PLATELETS
o CONTRACT AND PULL WALLS TOGETHER
o DEGRANULATION
PLATELET PLUG FORMATION
* DEGRANULATION
o RELEASE OF COMPOUNDS TO
+ VASOCONSTRICT
+ ATTRACT PLATELETS
+ STIMULATE DEGRANULATION
+ PROMOTE AGGREGATION
o POSITIVE FEEDBACK
CONTROL OF BLEEDING
* COAGULATION (CLOTTING)
* MOST EFFECTIVE DEFENSE
* FIBRINOGEN  FIBRIN  POLYMER
* TWO REACTION PATHWAYS
o EXTRINSIC MECHANISM
+ CLOTTING FACTORS FROM DAMAGED BLOOD VESSEL
o INTRINSIC MECHANISM
+ CLOTTING FACTORS FROM BLOOD
CLOTTING FACTORS
* PROCOAGULANTS
* PROTEINS PRODUCED IN LIVER
* INACTIVE  ACTIVE
o EACH ACTIVATES THE NEXT
o REACTION CASCADE
o AMPLIFICATION AT EACH STEP
o POSITIVE FEEDBACK INVOLVED
* CLOT RETRACTION
o CLOT FORMED
o PLATELETS ADHERE TO FIBRIN
o PLATELETS CONTRACT
o PULLS EDGES OF BROKEN VESSEL TOGETHER
* PLATELETS SECRETE PDGF
o PLATELET-DERIVED GROWTH FACTOR
o STIMULATES MITOSIS
* FIBROBLASTS INVADE AND PRODUCE CONNECTIVE TISSUE

CLOT DISSOLUTION
* FIBRINOLYSIS
* MULTIPLE STEPS
* POSITIVE FEEDBACK
* SIMILAR, IN REVERSE
PREVENTION OF COAGULATION
* PLATELET REPULSION
* DILUTION AND BLOOD MOVEMENT
* ANTICOAGULANTS
o ANTITHROMBIN (LIVER)
o HEPARIN (BASOPHILS)

COAGULATION DISORDERS
HEMOPHILIA

* DEFICIENCY IN A CLOTTING FACTOR
* CASCADE DISRUPTED
* CLOTTING DEFICIENCY
COAGULATION DISORDERS
HEMOPHILIA A
COAGULATION DISORDERS
HEMOPHILIA B
BLOOD CELL PRODUCTION
STEM CELLS
* PLURIPOTENT CELLS
o UNDIFFERENTIATED CELLS
o ABLE TO DIVIDE AND DIFFERENTIATE INTO MULTIPLE TYPES OF CELLS
o NOT ALL ARE “TOTIPOTENT”
o (NOT FULLY DIFFERENTIATED)
o E.G., HEMOCYTOBLASTS (BLOOD)
o E.G., EMBRYONIC STEM CELLS
* YOLK SAC
o EARLIEST HEMOPOIETIC TISSUE
o PRODUCES STEM CELLS
o COLONIZE OTHER ORGANS
+ BONE, LIVER, SPLEEN, THYMUS, ETC
o LIVER STOPS HEMOPOIESIS AT BIRTH
o SPLEEN STOPS ERYTHROPOIESIS SHORTLY AFTER BIRTH
* MYELOID HEMOPOIESIS
o OCCURS IN BONE MARROW
o FORMS ALL SEVEN FORMED ELEMENTS
* LYMPHOID HEMOPOIESIS
o OCCURS IN SEVERAL ORGANS
+ THYMUS, TONSILS, LYMPH NODES, SPLEEN, INTESTINES, ETC.
o PRODUCES LYMPHOCYTES
HEMOCYTOBLASTS
* STEM CELLS
* PLURIPOTENT
* DIFFERENTIATE INTO ALL FORMED ELEMENTS
o ERYTHROPOIESIS
o LEUKOPOIESIS
o THROMBOPOIESIS

ERYTHROCYTE PRODUCTION
ERYTHROPOIESIS
ERYTHROCYTE PRODUCTION
ERYTHROPOIESIS
ERYTHROCYTE HOMEOSTASIS
IRON METABOLISM
ERYTHROCYTE DEATH
HEMOLYSIS
* IRON
* PORPHYRIN RING
LEUKOCYTE PRODUCTION
LEUKOPOIESIS
PLATELET PRODUCTION
THROMBOPOIESIS
PLATELET PRODUCTION

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Venous Thromboembolic Disease

VENOUS THROMBOEMBOLIC DISEASE
by:R. Duncan Hite, MD
Section on Pulmonary and Critical Care Medicine

Venous Thromboembolic Disease

* Venous thrombosis - ~ 5 million pts yearly
+ Most caused by inadequate prophylaxis in hospitalized pts
* 10 % suffer pulmonary embolism ~ 500,000
* ~ 1% of all hospitalized pts have PE
* Contributes to 6 % of all hospital deaths
* ~ 125,000 deaths annually from PE
+ 3rd most common cardiovascular cause of death (MI, CVA)
+ Most deaths occur early – PREVENTION IS KEY!!
* Diagnosis of PE made in < 30% when contributes to death; < 10% if incidental

Case studies
Venous Thromboembolic Disease
Epidemiology

* 85 - 90% of PE pts have DVT risk factors
* 90-95% of PEs arise from lower ext. DVT
* Defined DVT Risk Factors: (Virchow’s Triad)
o Venous stasis - CHF, Immobility, Age > 70, Travel, Obesity, Recent surgery (4 weeks) or hospitalization (6 mos)
o Venous Injury - Prior DVT/PE, LE Trauma/Surgery
# LE trauma or surgery - Very high (50+%)
# Major surgery - (5 - 8%)
o Hypercoaguability - Cancer, Pregnancy, Nephrotic Syndrome, Hyperhomocysteinemia, Factor V Leyden mutation, Deficiency of Protein C/S or ATIII, Anti Phospholipid Ab, HITTS, Smoking

Pulmonary Hypertension Hemodynamic Effects
Deep Venous Thrombosis
Diagnosis
* Venography - remains the “gold standard”
+ Pitfalls: Difficult to perform, expensive, contrast load, DVT
* Compression Ultrasound (Sonography, Duplex and Color Doppler)
+ Criteria: echogenicity, noncompressibility, distension, free floating thrombus, absence of Doppler waveform, Abnormal color image
+ Accuracy:
# Symptomatic Patients: Sensitivity = 90-100%, Specificity = 95-100%
# High Risk Asymptomatic: Sensitivity = 50-80%, Specificity = 95-100%
* Impedance Plethysmography
* Radionuclide Venography (Indium-111)
* MRI - increasing popularity and utilization, includes deep pelvic veins

Deep Venous Thrombosis Prevention
* Orthopedic Surgery
o LMWH or Coumadin (INR 2.0 - 3.0) beginning preoperatively or immediately postoperatively. Adjusted dose SQ Heparin is an acceptable alternative but more complex.
o Adjuvant use of mechanical devices may add additional benefit. May be sufficient as primary prophylaxis for TKR if used optimally.
o Low dose SQ Hep, Aspirin, IPC alone are not recommended (less effective).
o Duration:
+ minimum of 7-10 days
+ Post Discharge Prophylaxis: 4-6 weeks for high risk patients
* General Surgery (including Urologic)
o Prophylaxis with SQHep, LMWH, ES or IPC
+ Moderate Risk - minor procedure with a risk factor or 40-60 yo, major procedures and <40
+ High Risk - minor procedure with risk factors or >60, major procedures with risk factors or age >40.
+ Increased Risk of Bleeding - use ES or IPC
o Combination therapy: very high risk - multiple risk factors
o Postdischarge Prophylaxis: selected very high risk pts
* Gynecologic Surgery
o Major surgery for benign disease
# SQ Hep BID, LMWH, IPC, continue for several days post op
o Major surgery for malignancy
# SQ Hep TID, Combination AC/Mech, high dose LMWH
* Neurosurgery
o Intracranial Surgery
# IPC or ES, Low dose SQHep or LMWH may be acceptable
# Combination IPC or ES with SQHep or LMWH in high risk

Deep Venous Thrombosis Prevention
* Trauma
o LMWH as soon as possible
o IPC or ES until LMWH started
* Acute Spinal Cord Injury
o LMWH recommended
o Low dose SQHep, ES or IPC are less effective
o Combination Mechanical/anticoagulant may be acceptable
o Continue throughout rehabilatation
* Medical (Cancer, CHF, Bedrest, MI, CVA…)
o Low dose SQ Hep or LMWH
o IPC if anticoagulation contraindicated

PE SIGNS AND SYMPTOMS
Symptoms
* Dyspnea - 80%
* Chest pain - 70%
* Cough - 50%
* Apprehension - 50%
* Hemoptysis - 30%

Signs
* Tachycardia - 60%
* Tachypnea - 70%
* Fever - 60%
* Clinical DVT - 30%

Pulmonary Embolism Diagnosis
* Chest x-ray - nonspecific abnormalities in most; normal early
+ Westermark's sign and Hampton's hump uncommon
* Arterial blood gas – hypoxemia is common
+ 15 - 20% will not manifest hypoxemia (i.e. normal A-a gradient)
* ECG – nonspecific changes typically
+ S1Q3T3 pattern in massive PE with RV strain
+ helpful in evaluating other causes of chest pain

PE – V/Q LUNG SCAN
* Radiolabeled Xenon inhaled for ventilation and radiolabeled Technetium for perfusion
* Safe
* Not very specific
* Not very useful if pre-existing lung disease

Pulmonary Embolism Diagnosis - V/Q Scan
Pulmonary Embolism
Diagnosis - Pulmonary Arteriogram
* Remains “gold standard” for Dx of PE
* Expensive
* Low morbidity and mortality
o Mortality < 0.1%
o Major morbidity < 0.5%
o Pulmonary Hypertension not a contraindication
Pulmonary Embolism
Diagnosis - Pulmonary Arteriogram
Lobar Defect
Segmental Defect
Pulmonary Embolism
Diagnosis - Chest CT
* Accurate for segmental or larger PE
+ Sensitivity 85 - 95% (Overall 50-60%)
+ Specificity 90 - 100%
* Accuracy depends on interpreter
+ Large Inter-interpreter variability
+ Reduced accuracy with less experience
* Significant contrast load ~ 65% of PA gram
* Similar expense to Pulmonary Arteriogram
* Can identify other pulmonary etiologies
Pulmonary Emboli Diagnosis - MRA
Venous Thromboembolism Treatment
Continuous IV Heparin:
Heparin-Induced Antibodies
Venous Thromboembolism Treatment
Low Molecular Weight Heparins:
Venous Thromboembolism Outpatient LMWH
Enoxaparin sodium
Unfractionated heparin
Venous Thromboembolism
Treatment
Synthetic Heparins:
Fondaparinux (Arixtra)
Oral anticoagulation (Coumadin)
Inferior Vena Cava Filter

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Approach to the Jaundiced Patient

Approach to the Jaundiced Patient
Internal Medicine Survivor Series
By:Joel Bruggen, MD

New Onset Jaundice
* Viral hepatitis
* Alcoholic liver disease
* Autoimmune hepatitis
* Medication-induced liver disease
* Common bile duct stones
* Pancreatic cancer
* Primary Biliary Cirrhosis (PBC)
* Primary Sclerosing Cholangitis (PSC)

Jaundiced Emergencies
* Acetaminophen Toxicity
* Fulminant Hepatic Failure
* Ascending Cholangitis

Jaundice Unrelated to Intrinsic Liver Disease
* Hemolysis (usually T. bili < 4)
* Massive Transfusion
* Resorption of Hematoma
* Ineffective Erythropoesis
* Disorders of Conjugation
o Gilbert’s syndrome
* Intrahepatic Cholestasis
o Sepsis, TPN, Post-operation

New Onset Jaundice
* Viral hepatitis
* Alcoholic liver disease
* Autoimmune hepatitis
* Medication-induced liver disease
* Common bile duct stones
* Pancreatic cancer
* Primary Biliary Cirrhosis (PBC)
* Primary Sclerosing Cholangitis (PSC)

HBV Serology
Resolved HBV
HBV vaccinated
Chronic HBV
Acute HBV
HBSAb
HBcAb
IgG
HBcAb
IgM
Acute Hepatitis C
HCV RNA
Anti-HCV
Infection Day 0
HCV RNA Day 12
HCV Antibody Day 70
Plateau phase = 57 days

Alcoholic Liver Disease
* The history is the key – 60 grams/day
* Gynecomastia, parotids, Dupuytren’s
* Lab clues: AST/ALT > 2, MCV > 94

AST < 300
* Alcoholic hepatitis:
o Anorexia, fever, jaundice, hepatomegaly
o Treatment:
+ Abstinence
+ Nutrition
+ Consider prednisolone or pentoxifylline

Alcoholic Liver Disease
Discriminant Function Formula:
DF = [4.6 x (PT – control)] + bilirubin
Consider treatment for DF > 32
* Prednisolone 40 mg/day x 28 days
o contraindications: infection, renal failure, GIB
* Pentoxifylline 400 mg PO tid x 28 days

Autoimmune Hepatitis
* Widely variable clinical presentations
o Asymptomatic LFT abnormality (ALT and AST)
o Severe hepatitis with jaundice
o Cirrhosis and complications of portal HTN
* Often associated with other autoimmune dz
* Diagnosis:
o Compatible clinical presentation
o ANA or ASMA with titer 1:80 or greater
o IgG > 1.5 upper limits of normal
o Liver biopsy: portal lymphocytes + plasma cells

Drug-induced Liver Disease
* Hepatocellular
o acetaminophen, INH, methyldopa, MTX
* Cholestatic
o chlorpromazine, estradiol, antibiotics
* Chronic Hepatitis
o methyldopa, phenytoin, macrodantin, PTU
* Hypersensitivity Reaction
o Phenytoin, Augmentin, allopurinol
* Microvesicular Steatosis
o amiodarone, IV tetracycline, AZT, ddI, stavudine

Acetaminophen Toxicity
* Danger dosages (70 kg patient)
o Toxicity possible > 10 gm
o Severe toxicity certain > 25 gm
o Lower doses potentially hepatotoxic in:
+ Chronic alcoholics
+ Malnutrition or fasting
+ Dilantin, Tegretol, phenobarbital, INH, rifampin
+ NOT in acute EtOH ingestion
+ NOT in non-alcoholic chronic liver disease

Acetaminophen Toxicity
* Day 1:
o Nausea, vomiting, malaise, or asymptomatic
* Day 2 – 3:
o Initial symptoms resolve
o AST and ALT begin to rise by 36 hours
o RUQ pain, tender enlarged liver on exam
* Day 4
o AST and ALT peak > 3000
o Liver dysfunction: PT, encephalopathy, jaundice
o Acute renal failure (ATN)

Acetaminophen Toxicity Treatment
Indications for NAC therapy:
Fulminant Hepatic Failure
* Definition:
o Rapid development of hepatic dysfunction
o Hepatic encephalopathy
o No prior history of liver disease
* Most common causes:
o Acetaminophen
o Unknown
o Idiosyncratic drug reaction
o Acute HAV or HBV (or HDV or HEV)

Fulminant Hepatic Failure
* Close glucose monitoring IV glucose
* Avoid sedatives - give PO lactulose
* Avoid nephrotoxins and hypovolemia
* Vitamin K SQ
o Do not give FFP unless active bleeding, since INR is an important prognostic factor
* GI bleed prophylaxis with PPI
* Transfer all patients with FHF who are candidates to a liver transplant center

Indications:
* Hepatitis C 29%
* Alcoholic Liver Disease 15%
* Cirrhosis of unknown etiology 8%
* Hepatocellular Carcinoma 7%
* Fulminant Hepatic Failure 6%
* Primary Sclerosing Cholangitis 5%
* Primary Biliary Cirrhosis 4%
* Metabolic Liver Disease 4%
* Autoimmune Hepatitis 3%
* Hepatitis B 3%

Liver Transplantation:
Contraindications
* ABSOLUTE
o active alcohol or drug abuse
o HIV positivity
o extrahepatic malignancy
o uncontrolled extrahepatic infection
o advanced cardiopulmonary disease
* RELATIVE
o Age over 65
o poor social support
o poorly controlled mental illness

Obstructive Jaundice
CBD stones (choledocholithiasis) vs. tumor
* Clinical features favoring CBD stones:
o Age < 45
o Biliary colic
o Fever
o Transient spike in AST or amylase
* Clinical features favoring cancer:
o Painless jaundice
o Weight loss
o Palpable gallbladder
o Bilirubin > 10

Ascending Cholangitis
* Pus under pressure
* Charcot’s triad: fever, jaundice, RUQ pain
o All 3 present in 70% of patients, but fever > 95%
o May also present as confusion or hypotension
* Most frequent causative organisms:
o E. Coli, Klebsiella, Enterobacter, Enterococcus
o anaerobes are rare and usually post-surgical
* Treatment:
o Antibiotics: Levaquin, Zosyn, meropenem
o ERCP with biliary drainage

Ascending Cholangitis
Indications for Urgent ERCP
* Persistent abdominal pain
* Hypotension despite adequate IVF
* Fever > 102
* Mental confusion
* Failure to improve after 12 hours of antibiotics and supportive care

Obstructive Jaundice Malignant Causes
* Cancer of the Pancreas
* Cancer of the Bile Ducts (Cholangiocarcinoma)
* Ampullary Tumors
* Portal Lymphadenopathy

Primary Biliary Cirrhosis
* Cholestatic liver disease (ALP)
o Most common symptoms: pruritus and fatigue
o Many patients asx, and dx by abnormal LFT
* Female:male ratio 9:1
* Diagnosis:
o Compatible clinical presentation
o AMA titer 1:80 or greater (95% sens/spec)
o IgM > 1.5 upper limits of normal
o Liver biopsy: bile duct destruction
* Treatment: Ursodeoxycholic acid 15 mg/kg

Primary Sclerosing Cholangitis
* Cholestatic liver disease (ALP)
* Inflammation of large bile ducts
* 90% associated with IBD
o but only 5% of IBD patients get PSC
* Diagnosis: ERCP (now MRCP)
o No autoantibodies, no elevated globulins
o Biopsy: concentric fibrosis around bile ducts
* Cholangiocarcinoma: 10-15% lifetime risk
* Treatment: Liver Transplantation

Diagnosis of Immune-Mediated Liver Disease
Periductal concentric fibrosis
Unusual Causes of Jaundice
* Ischemic hepatitis
* Congestive hepatopathy
* Wilson’s disease
* AIDS cholangiopathy
* Amanita phalloides (mushrooms)
* Jamaican bush tea
* Infiltrative diseases of the liver
o Amyloidosis
o Sarcoidosis
o Malignancy: lymphoma, metastatic dz

Wilson’s Disease
* Autosomal recessive – copper metabolism
* Chronic hepatitis or fulminant hepatitis
* Associated clinical features:
o Neuropsychiatric disease
o Hemolytic anemia
* Physical exam: Kayser-Fleischer rings
* Diagnosis: ceruloplasmin, urinary Cu
* Treatment: d-penicillamine

Critical Questions in the Evaluation of the Jaundiced Patient
* Acute vs. Chronic Liver Disease
* Hepatocellular vs. Cholestatic
o Biliary Obstruction vs. Intrahepatic Cholestasis
* Fever
o Could the patient have ascending cholangitis?
* Encephalopathy
o Could the patient have fulminant hepatic failure?

Evaluation of the Jaundiced Patient HISTORY

* Pain
* Fever
* Confusion
* Weight loss
* Sex, drugs, R&R
* Alcohol
* Medications
* pruritus
* malaise, myalgias
* dark urine
* abdominal girth
* edema
* other autoimmune dz
* HIV status
* prior biliary surgery
* family history liver dz

Evaluation of the Jaundiced Patient PHYSICAL EXAM
* BP/HR/Temp
* Mental status
* Asterixis
* Abd tenderness
* Liver size
* Splenomegaly
* Ascites
* Edema
* Spider angiomata
* Hyperpigmentation
* Kayser-Fleischer rings
* Xanthomas
* Gynecomastia
* Left supraclavicular adenopathy (Virchow’s node)

Evaluation of the Jaundiced Patient LAB EVALUATION
* AST-ALT-ALP
* Bilirubin – total/indirect
* Albumin
* INR
* Glucose
* Na-K-PO4, acid-base
* Acetaminophen level
* CBC/plt
* Ammonia
* Viral serologies
* ANA-ASMA-AMA
* Quantitative Ig
* Ceruloplasmin
* Iron profile
* Blood cultures

Evaluation of the Jaundiced Patient
* Ultrasound:
o More sensitive than CT for gallbladder stones
o Equally sensitive for dilated ducts
o Portable, cheap, no radiation, no IV contrast
* CT:
o Better imaging of the pancreas and abdomen
* MRCP:
o Imaging of biliary tree comparable to ERCP
* ERCP:
o Therapeutic intervention for stones
o Brushing and biopsy for malignancy

Case studies

Approach to the Jaundiced Patient.ppt

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Managing Low Birth Weight and Sick Newborns

Managing Low Birth Weight and Sick Newborns

Advances in Maternal and Neonatal Health

Session Objectives
* To define essential elements of the care of sick newborns, including neonatal resuscitation
* To discuss best practices and technologies

Management of Newborn Illness

* Education of mothers to recognize danger signals
* Working with families to develop complication plan for newborns
* Early recognition and appropriate management of newborn illness

Minimum Preparation for ANY Birth
The following should be available and in working order:
* Heat source
* Mucus extractor
* Self-inflating bag of newborn size
* 2 masks (for normal and small newborns)
* 1 clock
* At least one person skilled in newborn resuscitation present at birth

Essential Care for All Newborns
Most newborns breathe as soon as they are born and only need:
* A clean and warm welcome
* Vigilant observation
* Warmth
* To be observed for breathing
* To be given to the mother for warmth and breastfeeding

Immediate Care of the Newborn: Warmth
* Lay newborn on mother’s abdomen or other warm surface
* Immediately dry newborn with clean (warm) cloth or towel
* Remove wet towel and wrap/cover newborn, except for face and upper chest, with a second towel/cloth

* Blood on newborn is not a risk to newborn, but is a risk to caregiver
* Bathe after 24 hours
* In areas with high HIV prevalence, consider bathing earlier to reduce risk of maternal-fetal transmission, and to reduce risk to caregiver and to other newborns

Immediate Care of the Newborn
* Assess breathing
* Keep head in a neutral position
* IMMEDIATELY assess respirations and need for resuscitation

Signs of Good Health at Birth
Objective measures
* Breathing
* Heart rate above 100 beats/minute
Subjective measures
* Vigorous cry
* Pink skin
* Good muscular tone
* Good reactions to stimulus
* Most important measure is whether newborn is breathing
* Assessing all of above delays resuscitation, if it is necessary.

Birth Asphyxia
* Definition: Failure to initiate and sustain breathing at birth
* Magnitude:
o 3% of 120 million newborns each year in developing countries develop birth asphyxia and require resuscitation
o An estimated 900,000 of these newborns die as a result of asphyxia

Steps in Resuscitation
* Anticipate need for resuscitation at every birth, be prepared with equipment in good condition
* Prevent of heat loss (dry newborn and remove wet clothes)
* Assess breathing
* Resuscitate:
o Open airway
+ Position newborn
+ Clear airway
o Ventilate
o Evaluate

Assess Breathing
Newborn crying?
Provide routine care
* Chest is rising symmetrically
* Frequency >30 breaths/min.
* Not breathing/ gasping
* Breathing < 30 or > 60 breaths/ min.

Immediately start resuscitation
Provide routine care
Open Airway
* Position newborn on its back
* Place head in slightly extend position
* Suction mouth then nostrils

Ventilate
* Select appropriate mask size to cover chin, mouth and nose with a good seal
* Squeeze bag with two fingers or whole hand, look for chest to rise
* If chest not rising:
o Reposition head and mask
o Increase ventilation
o Repeat suctioning

Evaluate
After ventilating for about 1 minute, stop and look for spontaneous breathing
If no breathing, breathing is slow (< 30 breaths/ min.) or is weak with severe indrawing
If newborn starts crying/breathing spontaneously
Continue ventilating until spontaneous cry/ breathing begins

* Stop ventilating
* Do not leave newborn
* Observe breathing
* Put newborn skin-to-skin with mother and cover them both

Harmful and Ineffective Resuscitation Practices
Practices to be avoided include:
* Routine aspiration of the newborn’s mouth and nose as soon as the head is born
* Routine aspiration of the newborn’s stomach at birth
* Stimulation of the newborn by slapping or flicking the soles of her/his feet: only enough stimulation for mildly depressed-delays resuscitation
* Postural drainage and slapping the back: dangerous
* Squeezing the chest to remove secretions from the airway
* Routine giving of sodium bicarbonate to newborns who are not breathing
* Intubation by an unskilled person
* Some traditional practices:
o Putting alcohol in newborn’s nose
o Sprinkling or soaking newborn with cold water
o Stimulating anus
o Slapping newborn

Infection Prevention for Resuscitation
* Handwashing
* Use of gloves
* Careful suctioning if using a mucus extractor operated by mouth
* Careful cleaning and disinfection of equipment and supplies
o Do not reuse bulb—difficult to clean, poses risk of cross infection
* Correct disposal of secretions

Documentation
Details of the re
Post-Resuscitation Tasks: Successful Resuscitation
Post-Resuscitation Tasks: Unsuccessful Resuscitation
Policy Decisions for Resuscitation
Principles of Success
Care of the Low Birth Weight Newborn
Care of the Preterm Newborn
Principles of Management for Low Birth Weight and Preterm Newborns
* Warmth
* Feeding
* Detection and management of complications (e.g., resuscitation, assisted respiration)

As for all newborns:
* Lay newborn on mother’s abdomen or other warm surface
* Dry newborn with clean (warm) cloth or towel
* Remove wet towel and wrap/cover with a second dry towel
* Bathe after temperature is stable

Warmth: Problem with Incubators
* Potential source of infection
* Often temperature controls malfunction
* Often share incubator for more than one newborn

Need alternative method: kangaroo care
Feeding
Early and exclusive breastfeeding
* Breastmilk = best nourishment
* Already warm temperature
* Facilitated by kangaroo care

Definition of Kangaroo Care
* Early, prolonged and continuous skin-to-skin contact between a mother and her newborn
* Could be in hospital or after early discharge

How to Use Kangaroo Care
* Newborn’s position:
o Held upright (or diagonally) and prone against skin of mother, between her breasts
o Head is on its side under mother’s chin, and head, neck and trunk are well extended to avoid obstruction to airways
* Newborn’s clothing:
o Usually naked except for nappy and cap
o May be dressed in light clothing
o Mother covers newborn with her own clothes and added blanket or shawl
* Newborn should be:
o Breastfed on demand
o Supervised closely and temperature monitored regularly
* Mother needs lots of support because kangaroo care:
o Is very tiring for her
o Restricts her freedom
o Requires commitment to continue

Effectiveness of Kangaroo Care
* Randomized controlled trial
* Conducted in three tertiary and teaching hospitals in Ethiopia, Indonesia and Mexico
* Study effectiveness, feasibility, acceptability and cost of kangaroo mother care when compared to conventional methods of care
Benefits of Kangaroo Care
* Is efficient way of keeping newborn warm
* Helps breathing of newborn to be more regular; reduce frequency of apneic spells
* Promotes breastfeeding, growth and extra-uterine adaptation
* Increases the mother’s confidence, ability and involvement in the care of her small newborn
* Seems to be acceptable in different cultures and environments
* Contributes to containment of cost— salaries, running costs (electricity, etc.)

Summary

* Skilled attendant
* Equipment available and working
* Begin resuscitation immediately
o Ventilate
o Reassess frequently
o Kangaroo care once successful

References

Managing Low Birth Weight and Sick Newborns.ppt

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Normal Newborn Care

Normal Newborn Care - Advances in Maternal and Neonatal Health

Normal Newborn Care
Session Objective
* Define essential elements of early newborn care
* Discuss best practices and technologies for promoting newborn health
* Use relevant data and information to develop appropriate essential newborn recommendations

Newborn Deaths
Essential Newborn Care Interventions
* Clean childbirth and cord care
o Prevent newborn infection
* Thermal protection
o Prevent and manage newborn hypo/hyperthermia
* Early and exclusive breastfeeding
o Started within 1 hour after childbirth
* Initiation of breathing and resuscitation
o Early asphyxia identification and management
* Eye care
o Prevent and manage ophthalmia neonatorum
* Immunization
o At birth: bacille Calmette-Guerin (BCG) vaccine, oral poliovirus vaccine (OPV) and hepatitis B virus (HBV) vaccine (WHO)
* Identification and management of sick newborn
* Care of preterm and/or low birth weight newborn

Cleanliness to Prevent Infection
* Principles of cleanliness essential in both home and health facilities childbirths
* Principles of cleanliness at childbirth
o Clean hands
o Clean perineum
o Nothing unclean introduced vaginally
o Clean delivery surface
o Cleanliness in cord clamping and cutting
o Cleanliness for cord care
* Infection prevention/control measures at healthcare facilities

Thermal Protection
* Newborn physiology
o Normal temperature: 36.5–37.5°C
o Hypothermia: < 36.5°C
o Stabilization period: 1st 6–12 hours after birth
+ Large surface area
+ Poor thermal insulation
+ Small body mass to produce and conserve heat
+ Inability to change posture or adjust clothing to respond to thermal stress
* Increase hypothermia
o Newborn left wet while waiting for delivery of placenta
o Early bathing of newborn (within 24 hours)

Hypothermia Prevention
* Deliver in a warm room
* Dry newborn thoroughly and wrap in dry, warm cloth
* Keep out of draft and place on a warm surface
* Give to mother as soon as possible
o Skin-to-skin contact first few hours after childbirth
o Promotes bonding
o Enables early breastfeeding
* Check warmth by feeling newborn’s feet every 15 minutes
* Bathe when temperature is stable (after 24 hours)

Early and Exclusive Breastfeeding
* Early contact between mother and newborn
o Enables breastfeeding
o Rooming-in policies in health facilities prevents nosocomial infection
* Best practices
o No prelacteal feeds or other supplement
o Giving first breastfeed within one hour of birth
o Correct positioning to enable good attachment of the newborn
o Breastfeeding on demand
o Psycho-social support to breastfeeding mother

Breathing Initiation and Resuscitation
* Spontaneous breathing (> 30 breaths/min.) in most newborns
o Gentle stimulation, if at all
* Effectiveness of routine oro-nasal suctioning is unknown
o Biologically plausible advantages – clear airway
o Potentially real disadvantages – cardiac arrhythmia
o Bulb suctioning preferred
* Newborn resuscitation may be needed
o Fetal distress
o Thick meconium staining
o Vaginal breech deliveries
o Preterm

Eye Care To Prevent or Manage Ophthalmia Neonatorum
* Ophthalmia neonatorum
o Conjunctivitis with discharge during first 2 weeks of life
o Appears usually 2–5 days after birth
o Corneal damage if untreated
o Systemic progression if not managed
* Etiology
o N. gonorrhea
+ More severe and rapid development of complications
+ 30–50% mother-newborn transmission rate
o C. trachomatis

Eye Care To Prevent or Manage Ophthalmia Neonatorum (continued)
* Prophylaxis
o Clean eyes immediately
o 1% Silver nitrate solution
+ Not effective for chlamydia
o 2.5% Povidone-iodine solution
o 1% Tetracycline ointment
+ Not effective vs. some N. gonorrhea strains
* Common causes of prophylaxis failure
o Giving prophylaxis after first hour
o Flushing of eyes after silver nitrate application
o Using old prophylactic solutions

Efficacy of Prophylaxis for Conjunctivitis in China
* Objective: To assess etiology of newborn conjunctivitis and evaluate the efficacy of regimens in China
* Design: November 1989 to October 1991 rotated regimens monthly: tetracycline, erythromycin, silver nitrate
* 302 (6.7%) infants developed conjunctivitis, most S. aureus (26.2%) and chlamydia (22.5%)
* Silver nitrate, tetracycline: fewer cases than no prophylaxis (p < 0.05), erythromycin: not significant

Prophylaxis for Conjunctivitis: Objective and Design
* Objective: To compare efficacy in prevention of nongonococcal conjunctivitis
* Design: Randomized control trial to compare erythromycin, silver nitrate, no prophylaxis
o Examined with test for leukocyte esterase and chlamydia trachomatis antibody probe 30–48 hours postpartum, 13–15 days later, and telephone contact up to 60 days of life
* Main outcome measured: conjunctivitis within 60 days of life and nasolacrimal duct patency

Prophylaxis for Conjunctivitis: Results and Conclusion

* Results: 630 infants
* 109 with conjunctivitis
o Silver nitrate vs. no prophylaxis: Hazard ratio 0.61 (0.39-0.97)
+ Chemical conjunctivitis with silver nitrate resolves within 48 hours
o Erythromycin vs. no prophylaxis: Hazard ratio 0.69 (not significant)
* Conclusion: Parental choice of prophylaxis, including no prophylaxis, is reasonable IF antenatal care and STD screening

Povidone-Iodine for Conjunctivitis: Objective and Design

* Objective: To determine incidence and type of conjunctivitis after povidone-iodine in Kenya
* Design: Rotate regimen weekly: erythromycin, silver nitrate, povidone iodine
* Results:
o Conjunctivitis:
+ Chlamydia in 50.5%
+ S. aureus in 39.7%
o More infections in silver nitrate than povidone-iodine, OR 1.76, p < 0.001
o More infections in erythromycin OR 1.38, p=0.001

Povidone-Iodine for Conjunctivitis: Conclusion
Povidone-iodine:
o Is good prophylaxis
o Has wider antibacterial spectrum
o Causes greater reduction in colony-forming units and number of bacterial species
o Is active against viruses
o Is inexpensive

Immunization
* BCG vaccinations in all population at high risk of tuberculosis infection
* Single dose of OPV at birth or in the two weeks after birth
* HBV vaccination as soon as possible where perinatal infections are common

Summary
The essential components of normal newborn care include:

* Clean delivery and cord care
* Thermal protection
* Early and exclusive breastfeeding
* Monitoring
* Eye care
* Immunization
References

Normal Newborn Care.ppt

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Infant Lung Disease and Associated Complications

Infant Lung Disease and Associated Complications
By:Mary P. Martinasek, BS, RRT
Director of Clinical Education
Hillsborough Community College

Respiratory Distress Syndrome
* RDS , formerly called Hyaline Membrane disease (HMD)
* Primary cause of respiratory disorders
* 70% preterm deaths, 30% neonatal deaths
* Etiology - deficiency in surfactant
o Premature pulmonary system

Risk Factors associated with RDS
* Less than 35 weeks gestation
* Maternal diabetes
* Hx of RDS in sibling
* White male
* PFC (Persistent Fetal Circulation)
* Prenatal maternal complication
* Abnormal placental conditions
* Umbilical cord disorders

Pathophysiology of RDS
Decreased surfactant
Surface Tension
Compliance
Stiffer Lungs
Wide spread atelectasis
Worsening V/Q
FRC
WOB
PaO2& __ PaCO2
Respiratory Acidosis
Capillary damage
Alveolar Necrosis
Clinical Signs of RDS
* Respiratory Rate > 60 bpm
* Grunting
* Retracting
* Nasal flaring
* Cyanosis
* Hypothermia
* CXR = underaeration, opaque, ground glass appearance

Treatment of RDS
* Maternal steroids
* Artificial surfactant therapy
* Adequate hydration
* Thermoregulation
* Goal = support the patient’s respiratory system while minimizing complications

Complication of RDS
* ICH occurs in 40% of < 1500 grams
* Barotrauma = pulmonary air leaks
* Infection
* PDA

Airleak Identification
Clinical Scenario
BPD
Pathophysiology of BPD
CXR in BPD
* Stage I
o First 3 days of life
o Ground glass appearance on x-ray
* Stage II
o 3 - 10 days
o Opaque, obscure cardiac markings
* Stage III
o 10 - 20 days
o Cyst formations
* Stage IV
o 28 days
o Increased lung density, larger cysts
Treatment of BPD
* Avoidance of factors that lead to development
* Adequate ventilatory humidification
* CPT and bronchodilators
* Fluid management
* Nutrition

Persistent Pulmonary Hypertension
Treatment of PPHN
* Nitric Oxide (NO)
* Hyperventilation
* Tolazoline
* Dopamine
* ECMO (extracorporeal membrane oxygenation
* High frequency ventilation
Reverse Jeopardy
* What color tank is NO?
* What color tank is NO2?

Transient Tachypnea of the Newborn
* TTN
* Aka RDS II
* Term infants delivered via cesarean section
* Signs of RDS
* CXR - streaky infiltrates
* R/O pneumonia
* Treatment

TTN x-ray
Meconium Aspiration Syndrome
* Term and Postterm infan
Diagnosis and Treatment
* Aspiration of meconium
* Classic sign of RDS
* Irregular densities on CXR
* Treatment
o Suction meconium
o Peep
o Low peak pressures
o Antibiotics
o amnioinfusion

MAS x-ray
Asphyxia
* Major complication is hypoxic-ischemic encephalopathy
o Periventricular leukomalacia
* Tubular necrosis of kidneys and GI effects
* Liver damage
* Lung damage
PVL
Wilson- Mikity Syndrome
* AKA - Pulmonary dysmaturity
* BPD lung changes in unventilated infant
* Signs
o Hyperpnea, cyanosis, retractions, hypercarbia, respiratory acidosis
* Treatment
o Supportive
o Ventilated to treat apnea
o O2 to treat hypoxemia
Air leak syndrome
PIE x-ray
Apnea
Central or Nonobstructive Apnea
* Apnea of prematurity
* Chemoreceptor sensitivity
* Arousal response
* Stimulation of airway reflexes
* Dysfunction of the respiratory centers
* Dysfunction of the ventilatory muscles
* Dysfunction of the peripheral nervous system
* Treatment = caffeine or theophylline
Obstructive apnea
* Anatomic abnormalities
* Pierre Robin Syndrome (micronathia)
* choanal atresia, laryngeal webs, vocal cord paralysis, enlarged tonsils and adenoids
* Treatment = pharmacologic agents, surgery

What is choanal atresia and what is the classic sign?
Pierre Robin Syndrome
What is this x-ray terminology for this condition?
Retinopathy of Prematurity
Pathophysiology
Treatment of ROP
Intracranial/Intraventricular
Hemorrhage
* ICH and IVH
* Majority of hemorrhages in neonate are periventricular/ Intraventricular (IVH)
* Preterm and Infants <1500 grams high risk
* Germinal matrix most common

IVH
Signs of germinal matrix bleeding
IVH Classifications
Complications/ Treatment of IVH

Infant Lung Disease and Associated Complications.ppt

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Neonatal Resuscitation

Neonatal Resuscitation
By:Mary P. Martinasek, BS, RRT
Director of Clinical Education
Hillsborough Community College

Asphyxia
* Hypoxia + Hypercapnia + Acidosis
* May lead to irreversible brain damage
* The necessity to resuscitate is related to the degree of asphyxia

Causes of fetal asphyxia
* Maternal hypoxia
* Insufficient placental blood flow
* Blockage of umbilical blood flow
* Fetal disorders

Primary vs. Secondary Apnea
* Primary
o Initial asphyxia
o Signs
+ Initial period of rapid breathing
+ Respiratory movements cease
+ Heart rate and bp drop
+ Neuromuscular tone diminishes

Secondary Apnea
* If no resuscitation and apnea continues
* Signs
o Deep gasping respirations
o Heart rate continues to decrease
o Blood pressure begins to fall
o Infant flaccid

* Primary
o Stimulation and oxygen will usually induce respirations

* Secondary
o Infant unresponsive to stimulation – must be resuscitated

Effects of asphyxia on the lungs
* Ineffective respirations cannot open alveoli
* Pulmonary Hypertension
* Pulmonary vasoconstriction
o Hypoxia, hypercarbia, acidosis

Persistent Fetal Circulation
known as PPHN

* Leads to further asphyxia
* Blood shunted
* CO2 remains high despite ventilation
o Indocin
o Ligation of PDA

Preparation for Resuscitation

* Anticipation of high risk delivery
* Proper equipment
* Trained personnel

Purpose of Resuscitation

* Reverse asphyxia before irreparable damage has occurred

ABC’s of Resuscitation

* A – Establish an open airway
o Position infant
o Suction mouth then nose
* B – initiate breathing
o Use tactile stimulation
o Use PPV if necessary

Resuscitation

* C – Maintain circulation
o Stimulate and maintain circulation
+ Chest compressions
+ drugs

Initial steps
* Dry the infant
* Warm the infant
* Position the infant
* Suction the infant
* Stimulate the infant

Next step
* Evaluate respirations
o If none or gasping , provide PPV with 100% O2 for 15-30 seconds
o If spontaneous respirations then evaluate HR
* After 15-30 seconds of PPV or evaluation of spontaneous respirations then:
* EVALUATE HEART RATE
* If HR is above 100 then reevaluate respirations and color
* If HR is less than 60 continue/start PPV and start compressions

Reassess
* After 30 seconds reassess
* HR greater than 60 stop compressions
* HR greater than 100 and breathing stop PPV
* Evaluate infant’s color
o Peripheral vs. central cyanosis
o What is acrocyanosis?

Thermoregulation
* Maintain a neutral thermal environment
* Possible causes of heat loss
o Radiant
o Evaporative
o Convective
o Conductive

Neonatal Resuscitation.ppt

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Global trends of neonatal, infant and child mortality

Global trends of neonatal, infant and child mortality: implications for child survival
By:Dr KANUPRIYA CHATURVEDI & Dr S.K CHATURVEDI

When are child deaths occurring?

What are under-fives dying of?
(excluding neonatal causes of death)

* Pneumonia
* Diarrhoea
* Malaria
* Measles
* HIV/AIDS

Malnutrition contributes to more than half of all under-five deaths
What are neonates dying of?
* Preterm births
* Severe infection
* Asphyxia
* Congenital anomalies
* Tetanus

INDIA’S SHARE OF GLOBAL BURDEN
SOLUTIONS EXIST

* A mix of community and facility-based interventions
* A mix of integrated child health approaches
* Integrated management of neonatal and child hood illnesses is proven tool

Goals of IMNCI
* Standardized case management of sick newborns and children
* Focus on the most common causes of mortality
* Nutrition assessment and counselling for all sick infants and children
* Home care for newborns to
o promote exclusive breastfeeding
o prevent hypothermia
o improve illness recognition & timely care seeking

Essential components of IMNCI
* Improve health and nutrition workers’ skills
* Improve health systems
* Improve family and community practices
Home visits for young infants: Schedule
Colour Coded Case Management Strategy
Other innovations in case
Innovations in therapy
* Single daily dose gentamycin
* How to treat at home when hospital admission is not feasible
* Counselling the mother to give oral drugs at home
* Clear recommendations for follow up
* Negotiated feeding counselling
What does IMNCI not provide at all or fully
* Antenatal care
* Skilled birth attendance
* Birth asphyxia management
* Improved health system management
* What can be rapidly added to IMNCI
* Inpatient care modules for first level referral hospitals
IMNCI Experience--Milestones
* Early 2002, GOI constituted an Adaptation Group
* In joint GOI-UNICEF review meeting in April 2002 GOI requested to experiment IMNCI in BDCS districts
* July 2002, First national 2 days planning meeting
* December 2002, pre-tested 8-days physician course material
* Early 2003 - adaptation of H&N workers module
* May 2003 – First field testing in Osmanabad followed by one in Shivpuri & content & methodology frozen
* Implementation started in Andoor PHC, Osmanabad in June 03 followed by Valsad district
* Follow-up training of supervisors in April 04 in Osmanabad
* Field trial for case registers initiated in late 2004
* Physicians courses from 2005 included community visit, facilitation technique and briefing on Health workers’ course
* First Facilitation technique course in Orissa in June 2005

Training Flow
Training: Strengths -- Contents Doable
Training Limitations: Contents
Key messages

* Maternal and newborn care and support is essential to achieve a substantial reduction in neonatal mortality
* Improving child survival requires coordinated action between maternal and child health, and other programme areas (e.g. EPI, NUT, RBM, HIV)
* IMCI is an effective delivery strategy for multiple child survival interventions (India has already incorporated newborn care)
* For substantive impact, strong community component must accompany the health system strengthening

Global trends of neonatal, infant and child mortality.ppt

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