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Revalida Flashcards
Revalida Flashcards
Revalida Flashcards
Asthma
o Acute Asthma Exacerbation p. 2
o Severe Asthma
Anaphylaxis/ Anaphylactoid reaction p. 9 List Of 30 Emergencies
Acute Abdomen
o Intestinal Obstruction in
3. Acute Asthma Exacerbation
6. Anaphylaxis/ Anaphylactoid Reaction Page |
Children 7. Intestinal Obstruction In Children
o Mechanical Intestinal
Obstruction
p. 13 10. Acute Abdomen 1
11. Acute Cholangitis
o Acute Cholangitis 14. Hypertensive Urgencies And Emergencies
o Acute Appendicitis 17. VTE
Hypertension 19. Severe Asthma
o Hypertensive Urgency p. 27 21. Pneumothorax
o HTN in Pregnancy 24. Adrenal Crisis/ Acute Adrenal Insufficiency
Venous Thromboembolism p. 37 25. Diabetic Ketoacidosis
Pneumothorax p. 47 26. Thyrotoxic Crisis. Thyroid Storm
Adrenal Crisis p. 51 27. Uremic Emergency
Diabetic Ketoacidosis p. 54 29. Animal Bites (Dog, Cat, Rat)
Thyrotoxic crisis/ Thyroid storm p. 59 30. Tetanus
31. Inc. ICP
Uremic Emergency p. 63
36. Vaginal Bleeding In Pregnancy
Animal Bites (Dog, Cat, Rat)
p. 68 37. HTN In Pregnancy
Tetanus 5th ed
39. Head Trauma
Vaginal Bleeding in Pregnancy p. 75 41. Maxillo-Facial Injuries
Head trauma 42. Mech. Int. Obstruction
p. 84
o Increased ICP 43. Fractures
Fractures 44. Thermal Burns
p. 91
Maxillofacial injuries 45. Acute Urinary Retention
Thermal Burns 46. Foreign Matters Injury
p. 98
Thermal Injury 47. Ocular Trauma
Acute Urinary Retention p. 48. Epistaxis
o Urethral Catheterization 106 49. Foreign Bodies Of The Upper Aerodigestive
p. Tract
Foreign Matters Injury
111 50. Acute Appendicitis
p. 51. Thermal Injury
Ocular Trauma
120
p.
Epistaxis
129
p.
Foreign Bodies of the Upper Aerodigestive Tract
135
Page |
2
Asthma
3. Acute Asthma Exacerbation th
p. 42 6 ed
V. MANAGEMENT
IV. LABORATORY/ANCILLARY PROCEDURES
Goals of treatment:
CXR (PA and lateral)
o Rapid reversal of airway obstruction
o Not routinely done
o Correction of hypoxemia
o May show non-specific signs of hyperinflation
Importance of early intervention should have been emphasized to the patient
o Identify possible complications of airway obstruction
the longer it lasts, the worse it gets and the worse it gets, the longer it lasts Green zone Yellow zone Red zone
Well-controlled- Acute attack Emergency
Initial therapy should be directed at assessing the reversibility of bronchial obstruction
asymptomatic Mild to moderate attacks of asthma Severe or impending respiratory
using objective measures of pulmonary function arrest
Followed every day to Followed to prevent an asthma attack from
prevent most asthma getting worse
Beta-2 agonists
o Administered by nebulizations or metered-dose inhaler (MDI) with spacer
symptoms from
starting
Page |
o
6. Anaphylaxis/
Anaphylactoid
Reaction p. 65 6th ed
I. DEFINITION Vancomycin
1. Anaphylaxis Dextran
Life threatening IgE-mediated, antigen-induced reaction Anesthetic Agents
inciting allergen binds to specific IgE that has accumulated on previously sensitized Muscle relaxants
mast cells and basophils o Allergen extracts
massive release of biochemical mediators (histamines, leukotrienes, o Food, food additives Page |
o Venoms from insect stings and snake bites
prostaglandins, TXA and bradykinins)
clinical syndrome consisting of 2 or more of the ff organ involvement: o Latex
10
o Cutaneous/mucosal (90%)- flushing, urticaria, angioedema, pruritus o Physical factors: exercise-induced anaphylaxis
o Respiratory (70%)- laryngeal edema, bronchospasm, dyspnea, o Idiopathic (diagnosis of exclusion)
wheezing, stridor, hypoxemia
o GIT (40-50%)- n/v, crampy abd pain, diarrhea III. CLINICAL MANIFESTATIONS
o Cardiovascular (30-40%)- hypotension, tachycardia, syncope Anaphylaxis: 2 or more body systems are involved (cutaneous/mucosal, respiratory,
GIT and CV)
2. Anaphylactoid Reaction Within seconds or minutes of introduction of causative agent, occasionally within 1
Non-IgE mediated reaction hr
Do not require previous exposure symptom progression may be rapid or florid frequently associated with an
Involves one or more the ff mechanisms: impending doom
o complement activation mediators released from previously sensitized mast cells and basophils (histamines,
o direct mast cell activation (ie. Pharmacologic agents) leukotrienes, prostaglandins, TXA and bradykinins)
o alteration in arachidonic acid metabolism (ie. ASA, NSAIDs) o inc. mucous membrane secretions
Clinical picture is identical to anaphylaxis o inc. capillary permeability and leak
o dec. smooth muscle tone in blood vessels (vasodilation)
II. ETIOLOGIC AGENTS o inc. in smooth muscle tone of bronchioles
Pharmacologic agents: Laryngeal edema hoarseness, dysphonia, globus sensation (feeling of lump in
o Antimicrobials throat) upper airway obstruction
o Animal anti-sera/anti-toxin Nasal, ocular, palatal pruritus
o Other heterologous sera Sneezing
o Foreign proteins Diaphoresis
o (Causes anaphylactoid rxn) Disorientation
ASA Primary endangering aspects of acute systemic reactions (major symptoms)
NSAIDs o Cardiac dysfunction
Radiocontrast media o Hypotension
Opiates o Upper airway obstruction (ie. Laryngeal edema)
o Severe bronchial dysfunction, obstruction o Eating fish products that are not fresh and have been contaminated
In some pts, biphasic reactions may occur by bacteria resulting in formation of histamine
o Early anaphylaxis that resolve only to be ffd by a recurrence of Other causes of shock
anaphylaxis 72 hours later
VI. MANAGEMENT
IV. DIAGNOSIS Prevention is the best Page |
o Avoid agents known to cause anaphylaxis
Prompt recognition of the syndrome
o No definite lab work-up locally available to diagnose or confirm o Hx of drug allergy
11
anaphylaxis o Alternative drugs if theres (+) hx of allergy to drugs intended for
In vitro specific IgE tests or challenge tests or immediate hypersensitivity skin tests therapy
o Identify specific causes of anaphylaxis (food, medications, insects) o Do appropriate skin testing for heterologous sera & foreign proteins
Assay of the mast-cell derived preformed mediator tryptase o Administer drugs by oral route if feasible
o Used in some research centers to document massive activation of o Observe patients -1 hr after parenteral injection esp. IM penicillins
mast cells o Have patients with known drug allergy wear and carry warning
o Available in USA identification
o Instruct patients with prior history of life-threatening anaphylaxis on
V. DIFFERENTIAL DIAGNOSIS how to self-administer Epinephrine
Vasovagal collapse Monitor vital signs
o Occurs when a body overreacts to certain triggers, such as the sight Blocks action of histamine in peripheral tissues
of blood or extreme emotional distress. o Aqueous IM Epinephrine is given to a non-occluded extremity like the
o Causes a sudden drop in heart rate and blood pressure reduced lateral thigh (vastus lateralis muscle)
blood flow in the brain LOC 1:1000 at 0.01 mL/kg (max. 0.5mL) may be repeated
Hereditary angioedema every 5-15mins intervals
o Rare, autosomal dominantly inherited blood disorder that causes Given because absorption and subsequent
episodic swelling that may affect the face, extremeties, GIT and upper achievement of max. plasma concentration after SQ
airways admin is slower and may be significantly delayed with
o Entertained especially if theres (+) family hx shock
Arryhtmias, MI o Diphenhydramine 1mg/kg IV (slow over 20 sec) or IM every 4-6hrs
Aspiration thereafter
Pulmonary embolism o H2 blockers: Cimetidine 20-40mg/kg/day q6h (up to 300mg/dose) or
Seizures, panic attacks Ranitidine 1-2mg/kg/day every 6-8hrs IV (up to 50mg/dose)
Flushing disorders (alcohol ingestion) Corticosteroids (IV Methylprednisolone, IV Hydrocortisone, Oral Prednisone)
Post-prandial syndromes (eg. Scombroid poisoning) o Prevent late phase anaphylaxis
o IV Methylprednisolone 1-2mg/kg bolus then 2mg/kg/day divided q6h Glucagon 1-5mg (20-30mcg/kg, max 1 mg/dose in
(max 125mg/dose) children) IV over 5 min ffd by infusion (5-15 mcg/min)
o IV hydrocortisone 4mg/kg bolus then q6h (up to 100-200mg/dose) titrated to clinical response
o Oral Prednisone 1-2mg/kg/day up to 40-80mg/day q8-12h for a few o Theres bradycardia and bronchospasm induced by beta-blockade
days once anaphylaxis is under control Atropine 0.3-0.5 mg IV, repeat q10 mins (max 2mg
o Patients should still be monitored for 24 hrs for reccurence total dose in adults) Page |
Patients with hypotension Isoproterenol drip 0.1-1.5mcg/kg/min or starting dose
o Trendelenburg position, elevate lower extremities of 0.5mcg/min in adults and titrated accordingly
12
increase venous return to the heart, increase cardiac Patients with hypoxemia
output and improve organ perfusion o Oxygen on high-flow rates
current data to support the use of the Trendelenburg Removal of venom sac
position during shock are limited and do not reveal any o Dull edge of a knife
beneficial or sustained changes in systolic blood o Avoid compressing/squeezing
pressure or cardiac output. Patients with minor signs and symptoms, with marked resolution with emergency
o Rapid IV infusion with NSS treatment may be sent home
Correct 3rd space loss o Regular H1 blockers (anti-histamines)
5-10ml/kg as IV bolus during the 1st 3 mins of o With or without short course of Prednisone for 3-5 days
treatment o With proper instructions of follow-up care and emergency measures
Children: may receive up to 30ml/kg of IVF within 1 hr Patients with major life-threatening anaphylaxis
of treatment o Admitted and observed for another 24hrs in the hospital even if their
o Epinephrine infusion sx are managed and reversed in the ER because of risk of reccurence
Maintain BP of s and sx (late phase rxns) 8-24hrs after the initial manifestations
1mg Epi in 250ml D5W to yield 4mcg/ml at a rate of 1-
4mcg/min increased to a max of 10mcg/min
o Dopamine 400 mg in 500ml D5W to be infused at 2-20mcg/kg/min
Maintain a systolic BP >90mmHg
Patients with airway obstruction
o Not responding to Epinephrine
o Cricothyroidotomy
o Endotracheal Intubation
Patients on beta-blockers
o Switch to Calcium-channel blockers
Reduce bradycardia and bronchospasm
o Reverse beta-blockade:
10. Acute Abdomen
p.111 6th ed
Page |
13
7. Intestinal Obstruction in
Children p. 97 6th ed
Hypertension 27
17. Venous 37
Thromboembolism
p.212 6th ed
I. DEFINITION Immobility
Venous thromboembolism HF
o Formation of blood clots in the vein Obesity
o Encompasses DVT and PE Increased CVP
o Deep Vein Thrombosis o Hypercoagulability
Presence of thrombus on one of the deep venous Pregnant Page |
conduits that return blood to the heart OCP use
o Pulmonary embolism Coagulation disorders
38
Blockage of the main artery of the lung (or its Deficiencies of Protein C and S or
branches) by a substance from elsewhere in the AT III
body (embolism) Burns
Commonly results from venous thrombosis Malignancy
occurring in the deep veins of the lower o Intimal wall or endothelial injury
extremities Exposed collagen
Not a disease per se but is merely a complication stimulates local cytokine
of an underlying disease production and facilitates leukocyte
Massive PE (5-10% of cases) adhesion to the
Extensive endotheliumpromote venous
thrombosis affecting thrombosis
atleast half of the post-surgery
pulmonary after trauma
vasculature previous DVT
Submassive PE (20-25% of cases) Venous thrombi form in a venous valve (where eddy currents arise) or at a site
RV dysfunction of intimal injury
despite normal o 90% of cases of PE occur in the veins of the lower ext, usually
systemic arterial above the popliteal vein
pressure platelets aggregate release mediators initiate coagulation cascade
Low-risk PE (70-75% of cases) red thrombus
Have an excellent o Anytime during the formation of the red thrombus, the
prognosis thrombus can detach as an embolus
o Trigger very serious pulmonary and cardiac effects depending
II. ETIOLOGY/PATHOGENESIS on:
3 basic risk factors: Virchows Triad extent of reduction of the cross-sectional area of
o Stasis/Inflammation the pulmonary vascular bed
pre-existing status of the cardiopulmonary system o Palpable, indurated, cordlike, tender
o decreased gas exchange, increased vascular resistance subcutaneous venous segment
arterial hypoxemia, increased alveolar-arterial O2 tension o Variable discoloration of the LE
gradient o Blanched appearance of the leg because of edema
Increased anatomic dead space o Majority of the patients have no leg symptoms at the time of the
Breathed gas does not enter gas diagnosis Page |
exchange units of the lung Pulmonary embolism
Physiologic dead space increases o Dyspnea*
39
Ventilation to gas exchange units Most frequent symptom
exceeds venous blood flow through o Tachypnea*
the pulmonary capillaries Most frequent sign
o increased RV wall tension o Tachycardia
Interventricular septum bulges into and o Low-grade fever
compresses an intrinsically normal left o Neck-vein distention
ventriclereduces LV distensibility and impairs LV o Increase in the intensity of the pulmonic component of S2
filling o Massive PE
Compresses the RCA limits myocardial oxygen Dyspnea
supply RCA ischemia and RV microinfarction Syncope
underfilling of the LV decrease LV CO and Hypotension
systemic arterial pressure Cyanosis
III. CLINICAL MANIFESTATIONS o Small embolism near the pleura
DVT Pleuritic pain
o LE DVT is 10x more common than the UE DVT Cough
o Edema* Hemoptysis
Most specific symptom IV. DIAGNOSIS
o Cramp in the lower calf/charley horse* High index of clinical suspicion plus the presence of the major RF (Virchows
Most frequent symptom triad)
Non-specific o Reliable indicators of the likelihood of PE
Pain that persists and intensifies over several days No clinical findings are universal and absence of specific finding does not rule
o (+) Homans sign out the disease
Dorsiflexion of the foot calf pain Padua Prediction Score
o Superficial venous thrombosis o Identification of hospitalized patients at risk for VTE
o Warmth and erythema of the skin over the area of o Most widely used risk assessment tool to decide whether to
thrombosis administer VTE prophylaxis to these pts
o Cancer Wells Criteria
o Previous VTE o One of the most carefully tested clinical decision rules
o Immobility 1. s/sx of DVT
o Thrombophilia 2. Pulmonary embolism is more likely than alt. dx
o Trauma/surgery 3. Tachycardia
o >=70yo 4. Surgery/immobilization within last 4 weeks Page |
o Heart/resp. failure 5. Prior DVT or PE
o Acute MI or stroke 6. Hemoptysis
40
o Infection/rheumatic dx 7. Active malignancy
o Obesity o >=3pts: high likelihood of DVT
o Hormonal treatment o >=4pts: high likelihood of PE
o >=4pts: high risk of developing PE o Low-to-moderate likelihood of DVT (<3) or
American Academy of Family Physicians (AAFP)/ American College of Physicians (<4)PE D-dimer testing
(ACP) o High likelihood of VTE (>=3 for DVT or >=4 for
Recommendations for work-up of patients with probable DVT as PE) X D-dimer imaging
follows: New generation D-dimer assay + Wells criteria
o Validated clinical prediction rules (eg, Wells) Effective in ruling out clinically significant PE
should be used to estimate the pretest probability High negative predictive value (rule out test)
of venous thromboembolism (VTE) and interpret Quantitative Plasma D-dimer enzyme-linked immunosorbent
test results assay (ELISA)
o low pretest probability of DVT or PE Rises in the presence of VTE because of
o high-sensitivity D-dimer breakdown of fibrin by plasmin
o intermediate to high pretest probability of lower- Sensitivity:
extremity DVT >80% for DVT
o ultrasonography >95% for PE
o intermediate or high pretest probability of PE Not specific
o diagnostic imaging studies (eg, MI
ventilation-perfusion scan,
Pneumonia
multidetector helical CT, and
Sepsis
pulmonary angiography) are
Cancer
required
Post-operative state
2nd or 3rd trimester of pregnancy
o Cardiac Biomarkers low echogenecity
o Serum troponin Doesnt distinguish bet. old and new clot
o RV microinfaction Sen: 100%, spec: 99%
o Brain natriuretic peptide
o Myocardial stretch o ECG
o CBC o Not sensitive and specific Page |
o Leukocytosis o Enough to aid in the diagnosis of PE
o Coagulation studies (Prothrombin time, activated partial thromboplastin time) o Tachycardia
41
o Evaluate for hypercoaguable state o Non-specific ST-T wave changes
o ABG o Classic finding: S1-Q3-T3 pattern
o Decreased PO2 Observed only 20% of pts with proven PE
o Increased PCO2 o CXR
o Leg studies o Non-specific
o Hamptons hump
o Contrast Venography Peripheral wedge shaped infiltrate
Long been considered and remains the golden Assoc. with infarction
standard for dx of DVT o Westermarks sign
o Impedance Plethysmography (IPG) Decreased pulmonary vascular markings
Non-invasive test Decreased blood flow to a section of lung
Measures venous outflow from the lower ext o Pallas sign
Can detect proximal vein thrombosis Enlarged right descending pulmonary artery
Sen: 91%, spec: 96% o Lung scan
Detection of calf vein thrombosis is poor o V/Q scan
o Duplex scan o Second-line dx test for PE
Color Flow Doppler imaging o Used mostly for patients who cannot tolerate intravenous
Compression Ultrasonography contrast
Most widely used modality in evaluating pts with o Small particulate aggregates of albumin labeled with a gamma-
suspected DVT emitting radionuclide are injected intravenously and are trapped
Non-invasive test in the pulmonary capillary bed
Operator-dependent o Normal lung scan: virtually excludes the diagnosis of PE
Detects vein incompressibility o High-probability lung scan: high-likelihood of PE
most definite sign of thrombosis 2 or more segmental perfusion defects in the
o can also visualize thrombus presence of normal ventilation
homogenous
o Chest CT scan McConnells sign
o Principal imaging test for the dx of PE currently Hypokinesis of the RV free wall with
o Visualize the main, lobar and segmental PE hyperkinesis of the RV apex
o Pulmonary angiography
o Gold standard in dx PE before V. MANAGEMENT
o Reserved for patients DVT Page |
o with technically unsatisfactory chest CTs
o those whom an interventional procedure such as
Primary therapy
o Clot dissolution
42
catheter-directed thrombolysis is planned Low-dose catheter-directed thrombolysis
o (+): intraluminal filling defect or sharp cut-off of small vessels in Secondary prevention
more than 1 projection o Anticoagulation
o Secondary signs: o Placement of an Inferior Vena Cava filter
o Abrupt occlusion (cut-off) vessels o Compression stockings
o Segmental oligemia or a vascularity Pulmonary embolism
o Prolonged arterial phase with slow filling Risk stratification
o Tortuous tapering peripheral vessels o High risk of an adverse clinical outcome
o (-): exclude clinically relevant PE Hemodynamic instability
o MRI RV dysfunction on echocardiography
o MRI venography with Gadolinium contrast RV enlargement on chest CT
o Ultrasound is equivocal Elevation of troponin level
o MR pulmonary angiography o RV function remains normal in a hemodynamically stable patient
o May detect proximal large proximal PE but is not Good clinical outcome is high likely with
reliable for smaller segmental and subsegmental anticoagulant alone
PE Pulmonary embolism
o Sen: 85%, spec: 96% o Pharmacologic
Central, lobar and segmental emboli o Anti-coagulants
o Inadequate for the dx of sub-segmental emboli Mainstay of therapy for DVT
o Echocardiography Avoid further clot formation in the lower ext
o Bedside test Three options:
o Can reliably differentiate PE from other cardiac illness (MI, 1. Conventional strategy of parenteral
pericardial tamponade, dissection of aorta) therapy bridged to warfarin
o Transesophageal echocardiography (TEE) 2. Parenteral therapy bridged to a
indirect evidence of PE in pts with massive PE and novel oral anticoagulant such as
central emboli Dabigatran (direct thrombin
inhibitor) or Edoxaban (anti-Xa Greater
agent) bioavailability
3. Oral anti-coagulation with More predictable
Rivaroxaban or Apixaban (both are dose response
anti-Xa agents) with a loading dose Longer half-life
followed by a maintenance dose as More Less bleeding
Page |
monotherapy without parenteral
anticoagulation
complications 43
No lab monitoring or
3 heparin-based parenteral anticoagulants dose adjustment
1. Unfractionated Heparin (UFH) o Unless obese or
Initial drug of choice has CKD
Binding to and Enoxaparin 1mg/kg
accelerating the SQ q12h for up to 3
activity of mos in VTE pts with
antithrombin reversible risk
Monitor aPTT and factors
bleeding Recurrent emboli
complications and non-reversible
UFH bolus of factors
80IU/kg IV o Given
Maintenance indefinitely
infusion: 18 IU/kg 3. Fondaparinux
7-10 days (5 days is Anti-Xa
just as effective) pentasaccharide
aPTT maintained on Weight-based once
1.5-2 time the daily SQ
control No lab monitoring
Does not cause
2. Low-molecular-weight Heparin heparin-induced
(LMWH) (Enoxaparin) thrombocytopenia
Less binding to Adjusted downward
plasma proteins and for patients with
endothelial cells renal dysfunction
Suspected or proven heparin-induced Factor Xa inhibitor
thrombocytopenia Tx for DVT and PE as
Argatroban monotherapy
Bivalirudin w/o parenteral
Warfarin bridging
Vit K antagonist prevents anticoagulant
Page |
carboxylation activation of coag
factors 2, 7, 9 and 10
Dabigatran
Direct thrombin
44
Full effect requires at least 5 days inhibitor
If inititated as monotherapy during Edoxaban
an acute thrombotic illness Factor Xa inhibitor
Paradoxical Complications:
exacerbation of Hemorrhage
hypercoagulability Most serious AE of
increases the anticoagulation
likelihood of (Heparin or LMWH)
thrombosis Tx: Protamine
Overlapping UFH, LMWH, sulfate
Fondaparinux or parenteral direct Heparin-induced
thrombin inhibitors with warfarin thrombocytopenia
for at least 5 days will nullify the Less common with
early procoagulant effect of LMWH than with
Warfarin UFH
Monitor Prothrombin time (PT) Major bleeding
Target INR is usually 2.5, with a Warfarin
range of 2.0-3.0 Tx: Prothrombin
Novel Oral Anticoagulants Complex
Fixed dose concentrate
Establish effective anticoagulation Serious but non-life threatening
within hrs of ingestion bleeding
Require no lab monitoring Tx: FFP or IV Vit. K
Few drug-drug or drug-food Duration of anticoagulation
interactions DVT isolated to an UE or calf that
Rivaroxaban has been provoked by surgery,
trauma, estrogen or an indwelling rtPA 100mg administered as a continuous
central venous catheter or peripheral intravenous infusion over 2h
pacemaker the sooner it administered, the more effective it is
3mos used for at least 14 days after the PE has occurred
Provoked proximal leg DVT or PE Contraindications
3-6mos Page |
Intracranial disease
Pt with cancer and VTE
LMWH as
Recent surgery
Trauma
45
monotherapy w/o o Massive PE and hypotension
Warfarin o 500ml NSS
Continue Extreme caution because excessive
anticoagulation fluid administration
indefinitely unless exacerbates RV wall
the patients is stress
rendered cancer- causes more
free profound RV
Unprovoked VTE ischemia
Anticoagulation fro worsens LV
an indefinite compliance and
duration with a filling by causing
target INR 2-3 further
o Thrombolytic therapy (Recombinant Tissue Plasminogen interventricular
Activator- rTPA) septal shift toward
Accelerates resolution of clot the LV
Only FDA-approved indication for PE fibrinolysis: o Dopamine and Dobutamine
Massive PE First line inotropic agents for tx of
Dissolving much of the anatomically obstructing PE-related shock
pulmonary arterial thrombus o Other agents may include:
Prevents continued release of serotonin and other Norepinephrine
neurohormonal factors that exacerbate Vasopressin
pulmonary hypertension Phenylephrine
Lysing much of the source of the thrombus in the o Non-pharmacologic
pelvic or deep leg veins o Early ambulation
Esp for post-op pts
o Graduated classic compression stockings Active bleeding that precludes
Provide pressure to the LE to prevent venous anticoagulation
stasis Recurrent venous thrombosis
o Intermittent pneumatic compression (IPC) despite intensive anticoagulation
Mechanical device attached to an external Greenfield filter
machine which provides some form of passive leg Page |
Most popular and most widely used
exercises device
Stimulating muscle contraction VI. PROPHYLAXIS
46
o Pharmacomechanical catheter-directed therapy Important because VTE is difficult to detect and poses a profound
o Patients with relative CI to full-dose thrombolysis medical and economic burden
o Combines Low-dose UFH or LMWH
Physical fragmentation or o Most common in-hospital prophylaxis
pulverization of thrombus o UFH SQ q8h
Catheter-directed low dose o Enoxaparin 40mg SQ OD
thrombolysis prophylaxis and tx for pts with DVT with or
o Endovascular therapy without PE
o reduce the severity and duration of LE symptoms superior when compared to Aspirin
o prevent PE o Dalteparin and Fondaparinux- prophylaxis only
o diminish the risk of recurrent VTE
o Thrombus removal with catheter-directed Aspirin
thrombolysis o Recent studies have demonstrated its role as a venous
American College of Chest atithrombotic agent and potential use in VTE prophylaxis
Physicians (ACCP) recommends Patients who have undergone total hip or knee replacement or cancer
thrombolytic therapy only for surgery
patients with massive iliofemoral o Benefit from extended pharmacologic VTE prophylaxis
vein thrombosis associated with after hospital discharge (at least 1 month)
limb ischemia or vascular
compromise
o Mechanical thrombectomy
o Angioplasty
o Stenting of venous obstructions
o IVC interruption
2 principal indications for insertion of an IVC filter
Page |
47
21. Pneumothorax
p.176 6th ed
I. DEFINITION Cystic fibrosis
Pneumothorax o Neoplastic disease
o Collection of air or gas in the pleural space increases intrapleural Primary
pressure over-expansion of the hemithorax lung collapse Metastatic carcinoma
o Primary spontaneous pneumothorax o Interstitial lung disease
Occurs without antecedent trauma or iatrogenic causes Silicosis Page |
No apparent underlying disease or underlying conditions Fibrosing alveolitis/ interstitial pneumonitis
known to promote pneumothorax o Auto-immune disease
48
Family history and smoking are added risk factors Scleroderma
Tall, thin men, 20-40 yo RA
Believed to be caused by ruptured blebs or bullae o Trauma
Increased shear forces in the apex Blunt/crushing injuries
o Secondary spontaneous pneumothorax Penetrating injuries (fractured ribs, bullet/stab wounds)
Complication of an underlying pulmonary disease Barotrauma (pts on ventilators)
o Tension pneumothorax o Iatrogenic
Pulmonary or chest wall defect acts as a 1-way valve Barotrauma- increasing in ICU settings
Pleural pressure build-up which increases throughout the During CPR
breathing cycle lung collapse impedes venous Mechanical ventilation (esp. with PEEP)
return, prevents the heart from pumping blood Difficult endotracheal intubation
effectively During diagnosis and treatment interventions
o Bronchopleural fistula III. CLINICAL MANIFESTATIONS
Direct communication between the bronchus and pleura Dictated largely by:
persistent pneumothorax o Extent of the resulting lung collapse
II. ETIOLOGY AND RISK FACTORS o Presence of tension pneumothorax
Primary spontaneous pneumothorax o Severity of the underlying pulmonary disease, if present
o Ruptured apical pleural blebs/bullae Manifestations of the primary spontaneous pneumothorax are related to the
Secondary pneumothorax pneumothorax per se
o Infection Secondary spontaneous pneumothorax, other manifestation are related to the existing
PTB lung disease
Necrotizing pneumonias Sudden sharp chest pain exacerbated by cough, localized at the side of involvement
Hydatid cysts Dyspnea/ chest tightness
Pneumocytis carinii Anxiety, nasal flaring
o Airway obstruction Easy fatigability
COPD* Over-expansion of hemithorax
Lagging of affected side Chest CT scan
Hyperresonance over the affected side o Most reliable imaging study for diagnosing pneumothorax
Decreased breath sounds on the affected side o Not recommended for routine use
Midline shift to the opposite side o Rarely indicated but sometimes needed:
Cardiopulmonary failure to outline loculated pneumothoraces
o Marked dyspnea diff. pneumothorax from bullous lesions Page |
presence of SQ emphysema
o Cyanosis
o Hemodynamic instability obscures the x-ray
49
o Cognitive abnormality presence of interstitial lung disease
Tension pneumothorax V. TREATMENT
o Dyspnea Choice of intervention largely depends on:
o Tachycardia o Degree of lung collapse
o Distended neck veins o Clinical manifestations
o Hypotension o Presence of underlying lung disease
o Cyanosis o Presence of tension pneumothorax
o Diaphoresis o Problem of recurrences
o Changes in sensorium o Availability of local resources and expertise
Subcutaneous emphysema Goals:
o Swelling of the neck and face o Drain air from pleural space to re-expand the lung
o Feels as subcutaneous crepitations o Prevent recurrence
IV. DIAGNOSIS o Treat underlying disease
CXR Inhalation of high flow oxygen (10LPM)
o Diagnostic o Hastens fourfold the absorption of the pneumothorax
o Visceral pleural line with atelectasis and mediastinal shift to the Simple aspiration
opposite side o Steps:
o Existing lung disease 1. Asepsis around the 2nd ICS MCL, with pt slightly semi-
o SQ emphysema recumbent
o Pneumomediastinum 2. 1-2% Lidocaine is used to infiltrate the skin down to
ABG parietal pleura
o Impending or actual respiratory failure 3. Insert cannula (G14-16) through parietal pleura
o To assess: approximating chest wall thickness
Oxygenation 4. Connect the catheter to a three-way stopcock and may
Ventilator aspirate 2-3L gently
Acid-base status 5. Stop if resistance is felt and remove the catheter
6. Repeat CXR within 4 hours or sooner if the pt becomes
symptomatic again
o If theres bothersome cough or >3L has been aspirated
Catheter is retained and preferably attached to a chest
pump
o Reassess the need for a standard closed tube drainage if this attempt Page |
fails
Catheter drainage <=16Fr
50
Standard closed tube drainage
Video-assisted thoracoscopy (VATS) with stapling of blebs or leaks
o Recommended for persistent air leak of over 5 days or bronchopleural
fistula
Video-assisted thoracoscopic surgery with resection
Open thoracotomy with or without pleurectomy
o All modalities have failed
o Patient is a poor surgical risk
o Failure of lung to re-expand due to persistent air leak or bronchopleural
fistula
Pleurodesis
o Prevent recurrence
o Chemical (Tetracycline/Doxycycline)
o Mechanical abrasion under VATS
Page |
51
After stabilization
Decrease the IV PNSS rate
Search and treat for possible infections that can cause the adrenal crisis
Page |
25. Diabetic 54
Creatinine
CBC Adult patients
Its correction is the most urgent therapeutic priority
56
o leukocytosis o Isotonic Saline solution
CXR 15-20mL/kg/h or greater during the 1st hr
Electrocardiograph expand intravascular volume
Urinalysis restore renal perfusion
o Help in identifying the precipitating cause X heart failure
Diagnostic Criteria for DKA o Subsequent IVF replacement depends on:
State of hydration
DKA Serum electrolyte levels
HHS Urine output
Mild Moderate Severe
Plasma glucose (mg/dL) >250 >250 >250 >600 o 0.45% NaCl
7.25- 4-14mL/kg/h
Arterial pH 7.00-7.24 <7.00 >7.30 Given if corrected serum sodium is normal or elevated
7.3
Serum bicarbonate (mEq/L) 15-18 10-15 <10 >15 o Successful progress with fluid replacement is judged by:
Urine Ketones + + + small Hemodynamic monitoring
Effective serum osmolality BP
(mOsm/kg) Variable Variable Variable >320 Fluid input/output
2(Na+K)+Glucose/18 Clinical examination
Anion gap Pediatric patients
>10 >12 >12 Variable
(Na-(Cl+HCO3)) o The need for intravascular volume expansion must be offset by the higher risk of
Stupor/ cerebral edema associated with rapid fluid administration in children
Sensorium Alert Alert/drowsy Stupor/coma
coma o Isotonic Saline (0.9 NaCl)
Hyperosmotic Hyperglycemic State (HHS) 10-20mL/kg/h
Greater degree of dehydration and higher endogenous insulin secretion First hr of fluid administration
compared with DKA o Initial re-expansion should not exceed 50ml/kg over the first 4hr of therapy
Primarily seen in individuals with T2DM o Continued fluid therapy
Calculated to replace the fluid deficit evenly over 48hrs
o Monitor mental status Initially monitored hourly by a glucometer for
rapidly identify changes insulin drip dose adjustment
indicate iatrogenic fluid overload cerebral Multidose regimen of short and intermediate/long-acting insulin
edema Initiated based on:
Management o previous dose requirements
o Insulin therapy o total insulin dose of 0.6- Page |
Regular insulin
By continuous IV infusion
0.7U/kg/day
after resolution of DKA
57
Treatment of choice o glucose <200mg/dL
o Except in mild DKA o serum bicarbonate >=18mEq/L
IV bolus at 0.15U/kg followed by a continuous o pH >7.3
infusion of 0.1 U/kg/h o anion gap <12mEq/L
o Once hypokalemia (K <3.3mEq/L) is when patients are able to take fluids orally
excluded o Potassium
o Insulin bolus is not recommended in Decreases sodium potassium concentration
children Insulin therapy
Ideal rate of decrease in plasma glucose Correction of acidosis
concentration: Volume expansion
o 50-75mg/dL/h Potassium replacement
o If plasma glucose doesnt fall, 20-30mEq/L
insulin infusion may be doubled Initiated once serum level falls below 5.5 mEq/L
every hour Provided that theres adequate urine output
When plasma glucose reaches 250mg/dL Significant hypokalemia (<3.3mEq/L)
o Decrease the insulin infusion rate at Insulin treatment should be delayed until
0.05-0.1U/kg/h potassium concentration is restored
o Dextrose (5-10%) may be added to To avoid:
the IV fluids until acidosis is o Arrhythmias
resolved o cardiac arrest
Ketonemia typically takes longer to clear than o resp. muscle weakness
hyperglycemia o Bicarbonate
Blood should be drawn every 4-6hrs for determination of: Its use remains controversial
Serum electrolytes pH>7.0
Blood glucose reestablishing insulin activity
o blocks lipolysis
o resolves ketoacidosis Hyperchloremic Non-Anion Gap Acidosis
bicarbonate replacement is not necessary and is o Usually seen during the recovery phase of DKA
relatively contraindicated o Due to the loss of ketoanions plus excess infusion of chloride-containing fluids
pH6.9-7.0 during treatment
50mmol NaHCO3 + 200mL sterile water Arterial thrombosis
o Rate of 200ml/h o Manifesting as stroke, MI or an ischemic limb Page |
o
pH<6.9
100mmol NaHCO3 + 400mL sterile water Cerebral edema
Routine anticoagulation is not indicated
58
o Rate of 200mL/h o Direct complication of DKA
Pediatric patients o Children>adults
o 1-2mEq/kg over an hour o Associated with 20-40% mortality rate
o Can be added to NaCl o Raised ICP
o Phosphate Headache
Whole body phosphate deficits in DKA average ~1mmol/kg BW Mental status changes
Serum level decreases further with insulin therapy Papilledema
Studies have failed to show any beneficial effect of phosphate o Sudden deterioration in mental status after initial improvement in a patient with
replacement on the clinical outcome in DKA DKA
Overzealous phosphate therapy can cause severe hypocalcemia o CT scan
Phosphate replacement (20-30mEq/L Potassium phosphate) may Can establish the diagnosis
be sometimes indicated: o IV Mannitol
Cardiac dysfunction Helpful and may prevent neurologic sequelae
Anemia Lactic Acidosis
Resp. depression o Result from prolonged dehydration, shock, infection and tissue hypoxia
Serum phosphate conc <1mg/dL o Suspected in patients with refractory anion-gap metabolic acidosis despite
optimal therapy for DKA
VI. PROGNOSIS/PREVENTION Prevention
Most common complications: o Diabetes education should be reinforced at every opportunity with special
o Hypoglycemia emphasis on
Overzealous treatment with insulin Self-management skills during prodromal sick days
o Hypokalemia Bodys need for more, rather than less, insulin during such
Insulin and bicarbonate illnesses
o Hyperglycemia Testing of urine for ketones
Premature discontinuation of IV insulin Procedures for obtaining timely and preventive medical advice
failure to give subsequent SQ insulin once off IV insulin
Page |
Thyroid Storm
p. 163 6th ed
I. INTRODUCTION It occurs most frequently in young women (10 times more common in women
Thyroid hormone compared with men) at any age
o affects all organ systems II. ETIOLOGY/PATHOGENESIS
o responsible for increasing metabolic rate, heart rate, and ventricle Toxic diffuse goiter (Graves disease)- most cases
contractility, as well as muscle and central nervous system excitability Precipitating factors:
o Two major types of thyroid hormones are: o Infections
Page |
1. Thyroxine o
Thyroxine is the major form of thyroid o
Stress
Trauma
60
hormone. o Surgery
The ratio of thyroxine to triiodothyronine o DKA
released in the blood is 20:1. o Labor
Peripherally, thyroxine is converted to the o Heart disease
active triiodothyronine, which is three to o RAI treatment due to RAI thyroiditis
four times more potent o Withdrawal of anti-thyroid therapy
than thyroxine. o Vigorous thyroid palpation
2. Triiodothyronine o Salicylates
Hyperthyroidism precipitants multiply the effect of thyroid hormones by
o excess circulating hormone resulting only from thyroid gland o freeing thyroid hormones from their binding sites
hyperfunction o increasing receptor sensitivity.
Thyrotoxicosis Point at which thyrotoxicosis transforms to storm is controversial
o excess circulating thyroid hormone originating from any cause (including o No evidence that theres an increased production of T3 or T4 causing the
thyroid hormone overdose). storm
Thyroid storm o Magnitude of increase in thyroid hormones does not appear to be
o extreme manifestation of thyrotoxicosis. critical
o This is an acute, severe, life-threatening hypermetabolic state of Increased cathecholamine receptors have been noted
thyrotoxicosis caused either by excessive release of thyroid hormones Decreased binding to thyroid-binding globulin inc. free T3/T4
causing :
adrenergic hyperactivity or III. CLINICAL MANIFESTATIONS
altered peripheral response to thyroid hormone Similar to thyrotoxicosis but more exaggerated
o following the presence of one or more precipitants Fever- almost invariable and may be severe
o The mortality of thyroid storm Profuse sweating
without treatment: 80% and 100% Marked tachycardia of sinus or ectopic in origin
with treatment: 15% and 50%. Arrhythmias accompanied by pulmonary edema or CHF
Tremors
Restlessness ECG
Delirium or frank psychosis o usually abnormal
n/v, abd pain- early in the course o common findings are:
hypotension sinus tachycardia
coma and death- up to 20% of pts increased QRS interval
Apathetic hyperthyroidism P wave voltage Page |
nonspecific STT wave changes
o Impt to consider in elderly popn
atrial dysrhythmias
61
o Classic signs and sx of thyroid storm and thyrotoxicosis may be absent
IV. DIAGNOSTIC TESTS atrial fibrillation or flutter
Clinical diagnosis The diagnosis of thyroid storm is incomplete until a search for some cause of the crisis,
Scoring criteria (ie Burch and Wartofskys criteria) to confirm a thyroid storm especially infection has been made
Often confusing and not very impt since treatment is the same once suspected If the diagnosis of thyroid storm is high likely and patient is toxic immediate
May be useful in monitoring therapy treatment is indicated
Components: o If not, draw diagnostic tests and refer for further evaluation
1. Thermoregulatory dysfunction
2. CNS effects V. MANAGEMENT
3. GI-Hepatic dysfunction Goals of management:
4. Cardiovascular dysfunction o Stop synthesis of new thyroid hormones
>45- highly suggestive of storm o Halt release of preformed thyroid hormone
25-44- impending storm o Prevent conversion of T4 to T3
<25- storm unlikely o Control adrenergic symptoms associated with thyrotoxicosis
Free T4, T3 and TSH o Control systemic decompensation
o Treat underlying cause
CBC
Mnemonic: 3Ps
Serum Electrolytes
o PTU
Blood sugar
o Propanolol
o Electrolyte and glucose abnormalities may also be present due to
o Prednisone
gastrointestinal losses, dehydration, physiologic stress, and fever
Inhibit thyroid hormone formation and secretion
BUN
o Propylthiouracil 300-400mg q8h PO or by NGT
Liver function test
o Methimazole
Plasma cortisol
Preferred as first-line treatment unless contraindicated
Cranial CT scan
Avoided for pregnant women in first trimester as it can
o indicated for delirious or comatose patients
cause teratogenic effects
used in second and third trimester of pregnancy
o Sodium Iodide 1gm IV in 24h
Or Saturated Solution of Potassium Iodide 5 drops q8h
given 1-2hr after PTU
Sympathetic blockade
o Propanolol 20-40mg q4-6h Page |
CI:
Asthma
62
CHF that is not rate related
Prevent peripheral conversion of thyroxine to triiodothyronine
o Hydrocortisone 50-100mg IV q6h
Blocks thyroid release
Treat possible relative adrenal insufficiency from
hypermetabolism of steroids
Supportive therapy
o IVF
o Temperature control
Cooling blankets
Paracetamol
No Salicylates!
Competes with albumin binding
increases free thyroid hormone levels
Oxygen
Digitalis
For CHF
Decreased ventricular response
Treatment for the precipitating event
o Sedation and nutrition
VI. PREVENTION
Patients should be rendered euthyroid to mild
hyperthyroidism
Educated on the importance of compliance of their
antithyroid medications
Page |
63
27. Uremic
Emergency
p.192 6th ed
I. DEFINTION o Renal or Intrinsic: injury within the nephron unit
Uremic Emergency Acute tubular necrosis
o Presenting with renal failure, either acute or chronic Nephrotoxic
o with life threatening problems Vasculitis
hyperkalemia o Post-renal: urinary outflow obstruction
severe metabolic acidosis Prostatic disease Page |
cardiac arrhythmias Pelvic tumors
hypertension Intratubular crystalluria
64
renin hypersecretion Acyclovir
volume overload Retroperitoneal fibrosis
CHF Bilateral nephrolithiasis
Pulmonary edema Chronic renal failure
pericarditis o Diabetic nephropathy
pericardial effusion/tamponade o Hypertensive nephrosclerosis
encephalopathy o Chronic glomerulonephritis
o Lupus nephritis
II. ETIOLOGY o Chronic tubulointerstitial nephritis
Acute renal failure Gouty nephropathy
o Pre-renal: decreased renal perfusion Polycystic kidney disease
Hypovolemia Chronic pyelonephritis
Hemorrhage Chronic NSAID use
Dehydration o Usually assoc. with inadequate dialytic therapy for patients with end
Burns stage renal disease on renal replacement therapy (hemodialysis or
Cardiogenic shock peritoneal dialysis)
Sepsis o Acute component on top of an existing chronic renal failure:
Anaphylaxis Dehydration
Drugs Nephrotoxic drugs
ACEI Disease relapse
ARBS Disease acceleration
Infection
Diuretics
Decreased effective circulating volume from Obstruction
hypoalbuminemia Hypercalcemia
Hypocalcemia
Cirrhosis
Heart failure
Nephrotic syndrome
>10mmHg
III. CLINICAL MANIFESTATIONS Distant heart sounds
Ammoniacal breath Hypotension
Neurologic: May not be apparent because of long
o Apathy standing hypertension and hypertrophic
o Drowsiness cardiomyopathy Page |
o
o
Insomnia
Tremors
Gastrointestinal
o Anorexia
65
o Cognitive changes o n/v
o Asterixis may present with GI bleeding sec to. Uremic gastritis
o Disorientation aggravated by coagulopathy
o Restlessness
o Hallucination IV. LABORATORY/ANCILLARY PROCEDURES
o Seizures BUN
o Coma Serum Creatinine
o Lethargy Serum electrolytes
Pulmonary: o Sodium
o Edema o Potassium
o Pleural effusion o Calcium
o Kussmauls breathing (rapid and deep) Arterial blood gas
Secondary to metabolic acidosis CBC
Cardiovascular Urinalysis
o Uncontrolled BP CXR
o Arrhythmia UTZ of the kidneys
o Pericarditis o If obstruction is suspected
o Pleuritic chest pain 12L ECG
o Pericardial effusion o Pericarditis
Pericardial friction rub that can be hear throughout the Elevated ST segment in some leads without reciprocal
cardiac cycle or systole only depression in others followed by permanent or
o Cardiac tamponade temporary inversion of T waves
Presence of pulsus paradoxus 2D echo
an abnormally large decrease in systolic o If cardiac tamponade is suspected
blood pressure and pulse wave amplitude
during inspiration
V. MANAGEMENT o Diuretics
Hyperkalemia Loop and Thiazide diuretics
o Plasma K >=5.5mM Can be utilized to reduce K in
o First priority is assessment of need for emergency treatment followed by volume-replete or
comprehensive work-up hypervolemic patient with
ECG manifestations should be considered as an sufficient renal function Page |
emergency o Dialysis
Patients with plasma K levels of >=6.6, even without ECG Hemodialysis
66
changes, should be managed aggressively Most effective and reliable
Patients should be placed on continuous cardiac method to reduce plasma K
monitoring concentration
o Management is divided into stages: Metabolic Acidosis
1. Cardioprotection (from arrhythmic effects of o Sodium bicarbonate (NaHCO3)
hyperkalemia) o HCO3- deficit = deficit/L (desired serum HCO3- - measured HCO3-) 0.5
o 10% Calcium Gluconate 10mL/IV over 2-3 body weight (volume of distribution for HCO3-)
mins with cardiac monitoring Pulmonary edema
Calcium raises the action o Sit the patient up
potential threshold and o Assure oxygenation
reduces excitability without o Protect the airway
changing the resting o Furosemide 400-600mg/IV
membrane potential o Nitroglycerine 10-200ug/min
o Dose should be repeated if theres no o Morphine 5mg/IV
change in ECG findings or if they recur o Removal of fluid by dialytic therapy
2. Cellular Redistribution (shifts K inside cells) Hypertensive encephalopathy
o Regular insulin 10 u + D5050 o Protect airway
o Nebulized Salbutamol 10-20mg in 4mL o Check fundi, reflexes and coma score
PNSS inhaled over 10mins o Seizure precaution
3. Potassium Excretion o Graded reduction of blood pressure to avoid infarction
o Cation exchange resins Uremic encephalopathy
Sodium Polysterene Sulfonate o Protect airway
(SPS) o Choose mode of dialytic therapy
Exchanges Na for K in the GI Hemodialysis
tract and increases fecal K initial 2hrs with low blood flow
secretion
Peritoneal dialysis
less episode of disequilibrium
o Avoid disequilibrium
Pericarditis
o Daily dialysis
o Low heparin/ no heparin dialysis Page |
Cardiac tamponade
o Needle drainage before dialysis
67
avoid hypotension
o Low/no heparin dialysis
VI. PREVENTION
Increase frequency of dialysis for ESRD patients maintained on regular dialysis
Important to correct as many risk factors as possible
Avoidance of nephrotoxic medications in high risk patients
Prevention of additional insults (infection, dehydration, etc)
Maintenance of volume homeostasis with careful daily assessment of volume status
Potassium homeostasis
o Monitoring K levels
o Dietary restriction
Maintenance of acid-base homeostasis
Nutrition homeostasis
o Provide enough calories and protein to prevent development of
hypercatabolic state and maintain optimal nutrition status
Page |
68
V. PROGNOSIS
Factors associated with a worse outcome in adult tetanus:
o >70 yo
Page |
75
41. Maxillofacial
injuries
p. 336 6th ed
FRACTURES exposure; usually massively
contaminated
I. INTRODUCTION IIIC
Fracture o Open fracture with an arterial
o Break in the surface of a bone either across its cortex or through its articular injury that requires repair
surface regardless of size of soft tissue Page |
o Description depends on: wound
Integrity of soft tissue Stages of Bone Healing 92
Complete or incomplete 1. Impact
Displacement Enough energy is absorbed to induce failure of the bone
Fracture pattern Force exceeds the modulus of elasticity of the bone
Anatomic location 2. Induction
Regional location Begins with formation of fracture hematoma
o Accdg to integrity of soft tissue: Ends with appearance of inflammatory cells
Closed fracture Approximately occurs during the 1st 48hrs after the impact
Fracture surface does not communicate with Bone ends necrosis (at 48hrs)
skin or mucous membrane Low O2 tension and platelet (due to the hematoma)
Open fracture Release of chemical factors
Fracture where theres a communication 3. Inflammation
between the fracture and the skin or mucous Begins with influx of inflammatory cells
membrane with the external environment Ends with appearance of bone and cartilage production
o Classification: Gustilo and Anderson Osteoclast
Type I o Arrives to remove necrotic bones
clean wound Fibroblasts capillary ingrowth
<1cm long 4. Soft callus stage
Type II Characterized by development of cartilage (intramembranous)
Lacerations and bone
>1cm without extensive tissue damage Completed with cessation of appreciable fracture motion
Type III (clinical union)
IIIA Production of subperiosteal new bone
o extensive tissue lacerations or Fibrovascular stroma converted to chondroid matrix
flaps but maintain adequate o Stabilizes the fracture
tissue coverage of bone Usually occurs by the 2nd week
IIIB 5. Hard callus stage
o extensive soft tissue loss with Conversion of chondroid callus to woven bone
periosteal stripping and bony Endochondral ossification
At completion of this stage, fracture is considered healed IV. DIAGNOSIS
clinically and radiographically (radiographic union) History
Usually occurs by the 6th week o Detailed history concerning the nature of the accident and the mechanism of
6. Bone remodeling injury
Conversion of woven bone to lamellar bone PE
Medullary cavity and normal bone diameter are restored X-ray involving the extremity (AP and lateral views) Page |
Occurs after 1.5-2yrs o Should include the entire length of the injured bone and joints above and
below it 93
II. ETIOLOGY/PATHOGENESIS V. MANAGEMENT
Sudden injuries Closed
o Causative force producing the fracture may be o Treat first any life-endangering conditions before treating the fracture
Direct violence o Apply external mobilization through the use of cast or splint
MVA o Determine optimal treatment with either closed or open techniques of
Indirect violence reduction
Initial force is transmitted along the bone Methods of reduction:
break at some distance from the site of impact 1. Closed Reduction
Radial head is fractured in a fall of an Advantages:
outstretched hand Effectively uses the
Pathologic fractures natural repair processes
o Occurs in a bone already weakened by disease of the body
o Tumor Few complications
o Infection Disadvantages:
Fatigue fractures More difficult to perform
o Occurs as a result of repeated stress successfully
o Common in the bones of lower extremities Slight angulation and
shortening commonly
III. CLINICAL MANIFESTATIONS occur
Localized swelling 2. Open Reduction
Visible or palpable deformity Open skin, reduce manually, expose
Marked localized ecchymosis bone, reduce, align
Marked localized tenderness Disadvantages:
Preternatural abnormal mobility Delay in healing
o Absolute sign infection
Crepitus Open
o Treat all cases as an emergency
o Cover the wounds immediately with sterile dressing and splint the involved
extremity
Do not push the extruded soft tissue or bone back into the VI. PROGNOSIS
wound unless there is vascular compromise Complications
o Principles: o Infection
A. Prevention of infection o Implant failure
Emergency debridement (w/in 24 hrs) Before bone heals, implant cannot withstand forces impinging
Prophylactic broad spectrum antibiotics and breaks Page |
Anti-tetanus prophylaxis o Re-fracture
Culture & sensitivity study of the wound (ideally) o Non-union 94
B. Stabilization of fracture a. Immediate
Within 48hrs o Soft tissue injury
Casting/splints o Pulmonary complications
May cause irreversible muscle ischemia and destruction Fat emboli syndrome
Indications for OR and internal and external fixation: NOCAST o Compartment syndrome
Non-union Pressure from bleeding stop in the flow swelling
o No radiologic sign of healing increased intracompartmental pressure
after 6 mos) Common in trauma involving the leg, but can also be
Open fractures seen in the hand, foot and thigh
With vascular Compromise 5 Ps:
Displaced intra-Articular fracture Pain on passive motion
Special Earliest sign
o Pathologic fractures Pallor
o Failure of closed method Paresthesias
Poly-Trauma Paralysis
External fixators: for more severe injuries (type III) Pulselessness
Bone is contaminated Intra-compartmental readings: >30-40mmHg
Bacteria produce biofilm adhering to implants b. Late
decreases antibiotic efficacy o Delayed union
Internal fixators: for mild-moderate injuries (type I and II) o Malunion
C. Soft tissue coverage o Non-union
Reconstructive surgery: skin grafting, skin flaps, microvascular o Joint stiffness
free transfers o Post-traumatic arthritis
To protect bone o Avascular necrosis
Early soft tissue coverage, the better o infection
o External fixation
No plant foreign bodies
MAXILLOFACIAL TRAUMA o Fall
o Often limited to malar fractures only
I. INTRODUCTION Fractures from high velocity impact
Maxillofacial trauma o Vehicular accidents
o Injury to the facial region involving the soft tissue and facial skeleton o Often associated with fractures of other facial
o Result from accidental or deliberate trauma to the face bones Page |
o Most commonly fractured facial skeleton Classification:
Nose a. LeFort I/ Transverse/ Guerin Fractures 95
Zygoma Horizontal
Mandible Above the apices of the teeth
o Injuries to the midface usually results from Through the maxilla
vehicular accidents with passengers Associated with a blow in the upper lip
interpersonal violence b. LeFort II/ Pyramidal Fractures
May be closed or open fractures Fractures in the maxilla involving the nasal, lacrimal and
Fractures of the face ethmoidal bones and the zygomatico-maxillary sutures
o Upper third: from the roof of the orbit, going up Involves the buttresses and beams that maintain height, width
o Middle third: from the orbit, going down and projection of the face
o Lower third: mandible c. LeFort III Fractures
a. Upper third High transverse fracture of the maxilla
Less common: because of the protection of the nose (part o the middle third at the base of the nose and ethmoidal region, extending
of the face) across the orbits to the lateral rim
Nasal bone- most commonly fractured bone in the face separating the zygomatico-frontal suture
Highest morbidity and mortality due to the proximity to the brain complete separation of the facial bone structures from the
b. Middle third skull
Nasal is the most commonly fractured bone in the face mortality: assoc. with intracranial injury
Malar bone (Zygoma) being the second most common injury in the face c. Lower third
Attaches to the craniofacial by frontal, maxilla and temporal Mandible
projection Fairly strong bone
Form a tripod Great force must be exerted to break it
Maxilla
Presence of long-rooted teeth such as impacted molars and
Maintain vertical supports (paired bones) canines may change the direction of the angle where the
o Nasomaxallary vertical ramus meets the horizontal body, thereby greatly
o Zygomaticomaxillary weakening the mandible
o Pterygo-maxillary buttresses
Elderly edentulous patients
Two types of disruption are encountered:
o Atrophic bones and resorption of the
Fractures from low velocity impact alveolus fragile bones
o Punch
Condyle LeFort II/Maxillary fractures: malocclusion with anterior open
Most often fractured by indirect trauma bite/overbite (hallmark)
Particularly at its slender neck Mandibular fractures
2 groups of muscles that exert displacing forces on the fragments of Open into the mouth because of the presence of teeth
mandible
Posterior group: muscles of mastication; short, thick and III. DIAGNOSIS Page |
powerful X-ray of the mandible (AP, lateral and oblique views)
o Temporalis o Fracture of the body and ramus of the mandible 96
o Masseter o These may not give a good view of the condyles
o Medial and lateral pterygoids Panogram
Anterior group: pulls the mandible downward, posteriorly and o Will give a definite position of the condylar area
medially CT Scan
o Genioglossus o Will give a definite position of the condylar area
o Mylohyoid o Confirms diagnosis
o Digastric muscles o Help in planning of reconstructive management
Class I
Teeth are present on both sides of the fracture IV. MANAGEMENT
Class II Priority of treatment
Teeth are present on the side of the fracture and non- o Establishment and preservation of patients airway
edentolous teeth on the other o Airway may be blocked because of
Class III displaced palate and tongue
Edentulous mandible blood clots
Loss of alveolar ridge and bone atrophy loose teeth
bone fragments
II. CLINICAL MANIFESTATIONS foreign body
Peri-orbital ecchymosis broken dentures
Soft-tissue injuries o Do not lie patient flat on his back
Fairly common Avoid aspiration
May result from either deliberate or accidental trauma Prevents tongue from falling back on the
Bleeding airway
Usually alarming o Intubation
Sometimes out of proportion of the actual size of the o Control of hemorrhage
external injury o Not usually a problem in closed-type fractures
Malocclusion and mobility of the mid-face o Can be severe in open-type fractures
LeFort I: dental arches demonstrate an open bite, with superior Analgesics
displacement o X Morphine or Strong narcotics
o Decrease respiration
o May mask signs of head injury
Antibiotic therapy
o LeFort II or III
o CSF rhinorrhea
Anti-tetanus prophylaxis
o Initiated to start a course or as a booster dose Page |
Definitive treatment is never, in itself, life-saving
o Once the general condition of the patient permits, undue delay should be 97
avoided
o Surgeons objective
Return the patient to normal as possible with regards to
function and appearance
o Mandibular fractures
Aim of treatment: align the mandible in proper occlusion with
the opposing maxilla
o Maxillary fractures
Aim of treatment: reduce and immobilize the maxilla
Fixation is made to a sound bony point above
the level of the fracture and can be achieved by
internal skeletal fixation or by external rod and
cheek wires
Page |
44. Thermal Burns
ed
p.370 6th 98
V. PROGNOSIS
Complications:
o infection
Page |
111
the Upper
Aerodigestive Tract
p. 441 6th ed
I. INTRODUCTION May fragment
Inhalation or ingestion of foreign bodies Vegetable matter- most common airway foreign body
o Toddlers Nuts- most common food item aspirated
o Mentally retarded Seeds
o Alcohol-intoxicated adults Popcorn
o Children with preexisting esophageal abnormalities Hotdog Page |
o Airway o Non-organic materials
May lodge in the: Coins 136
Larynx Button batteries
Trachea Beads
Bronchus (80-90%) Candy wrapper
o Esophagus Airway foreign body is common among toddlers
Cricopharyngeal area (70%) o 70-80% are boys
Narrowest area o More common in toddlers
Cricopharyngeus sling (C6) They lack molars necessary for proper mastication of food
Thoracic inlet They have less controlled coordination in swallowing and
o Site of anatomical change from immaturity in laryngeal elevation and glottis closure
the skeletal muscle to the They have an age-related tendency to explore the
smooth muscle of the environment by placing objects in the mouth; grasping
esophagus becomes effective
Mid esophagus (15%) They are often running or playing at the time of accidental
Region where aortic arch and carina overlap ingestion
the esophagus o Location of the FB would depend on:
Lower esophageal sphincter (LES) (15%) Patients age
At the gastroesophageal junction (GEJ) Angles made by the mainstem bronchi with the
o American National Safety Council (1984) trachea are identical until age 15yo
rd
3 leading cause of death for infants o FB are found on either side with
4th leading cause of accidental death among toddlers (1-3yo) equal frequency in persons in
o P. Naugesa (2003) this age group
3rd leading cause of accidental death in children under 1 yr of As we grow older
age o Right bronchus becomes wider,
4th leading cause of death in children 1-6yo shorter and straighter than the
left
II. ETIOLOGY/PATHOGENESIS o Interbronchial septruism
May aspirate: projects to the left
o Organic materials Most FB aspirated are found in the right
Expand with moisture bronchi
Physical position at the time of aspiration 1st phase: Initial phase
o Larger objects tend to become lodged in the larynx or trachea occurs at the moment of aspiration
o Valve Action: impaction of foreign body
By-pass valve action manifestations:
occurs when the foreign body allows air to pass o Choking
during both inspiration and expiration o Gaggling Page |
Check-valve phenomenon o Paroxysm of cough
occurs when air can enter the lung during o Airway obstruction 137
inspiration, due to widening of the bronchus, 2nd phase: Asymptomatic phase
but cannot escape during expiration foreign body becomes lodged and reflexes
Net effect: alveolary hyperinflation fatigue
Ball-valve action Asymptomatic
air can leave but cannot enter rd
3 phase: Complications
resulting in atelectasis Obstruction, erosion and infection causes:
Stop-valve phenomenon o Pneumonia
occurs when the airway is completely blocked, o Atelectasis
during both inspiration and expiration o Abscess
Esophageal foreign body is common among adults o Fever
o Philippines o Clinical presentation depends on location of the FB
Dentures Laryngeal and tracheal foreign body
White part of balut Large FB can produce complete airway
o Singapore obstruction from either dimensions of the
Fishbone object or the resulting edema
o High-risk children Laryngeal FB
Esophageal stricture o Airway obstruction
Dysmotility syndrome o Hoarseness
Repaired tracheoesophageal fistula o Aphonia
o Usual locations of impactions are: Tracheal FB
Cricopharyngeus muscle along the esophagus o Present similarly to laryngeal FB
Level of the bifurcation of the trachea but without hoarseness or
Level of the diaphragm aphonia
o Presence of multiple foreign bodies suggest o Biphasic stridor
Anomalies (strictures and web) o Jackson-Jackson triad
Asthmatoid
III. CLINICAL MANIFESTATIONS wheeze
Airway foreign body Audible slap
o 3 clinical phases of aspirated foreign body:
Palpable thud on End of inspiration and expiration
the trachea Obliterated bronchial air column
Bronchial foreign body- most common (80-90%) Inspiratory hypoinflation or atelectasis
Classic triad: (65%) Expiratory hyperinflation
o Prolonged wheeze in the Emphysema
expiratory phase Lobar or segmental pneumonia Page |
o Discrepancy of breath sounds Localization of FB
between sides of the chest May not be seen in : 138
(decreased breath sounds on o 25% of bronchial
one side) o 50% of tracheal
o Cough Bilateral decubitus films
Unilateral wheezing o May be helpful in children
Hypersonority or dullness on percussion o FB may prevent normal
Hemoptysis pulmonary collapse when the
Esophageal foreign body involved hemithorax is
o Poor appetite and emesis dependent
o Adults and older children o Multidetector Computer tomography scanning (MDCT)
Dysphagia Detect presence of radiolucent vegetable FB
Odynophagia o Fluoroscopy
o Drooling Holzknecht-Jacobson phenomena
o Stasis of saliva in the hypopharynx Swinging mediastinum
Total obstruction Tracheal FB
o Proximal swallowing-related trauma Esophageal FB
Abrasions o Chest X-ray including the neck/abdomen in PA and lateral views
Streaks of blood Location
Edema in the hypopharynx Size of the FB
o Esophageal perforation Anticipate multiple FB
Fever with tachypnea Flat objects
Tachycardia Coronal plane on PA
Increased pain Parallel to the vertebral column on lateral film
IV. DIAGNOSIS Usually opaque
Airway FB Food products
o High-kilovolt (AP and lateral) radiographs of the airway 2nd most common
Test of choice May need barium esophagram
Produces greater definition of the airway while reducing the o Fluoroscopy with contrast
effect of the surrounding bony structures Esophageal perforation
o Chest and neck X-ray (PA and lateral) Extraluminal localization of the FB
o Fluoroscopy with thin barrier Successful in cases where in the FB is located at the LES
Required for non-radioopaque FB FB located in other areas of the esophagus are less likely to
V. MANAGEMENT spontaneously pass
Airway FB: Endoscopy and removal of foreign body o Esophagoscopy
o History and PE are the most important aspects in the decision for surgical Procedure of choice
intervention Both dx and tx Page |
Strong history of suspected FB aspiration prompts an Relatively invasive and expensive
endoscopic evaluation, even if the clinical findings are not as Indications: 139
conclusive Sharp objects
o Urgent or emergent endoscopy Caustic FB
Actual airway obstruction o Disc batteries- Cause local
Aspiration of dried beans or peas necrosis
o Laryngoscopy and Bronchoscopy Presence of resp. distress
Done asap Total esophageal obstruction
Should not precede patient preparation and proper o Reserved for previously healthy children whose ingestion of a blunt object
instrumentation was witnessed less than 24hrs prior to the procedure
Rigid Bronchoscope Foley catheter method
Procedure of choice for removing FB Patient is restrained in a head-down position
Larger diameter which facilitates the passage on a fluoroscopy table
of various grasping devices Uninflated catheter is inserted distal to the
Patient can be ventilated through the scope object
Indications: Catheter is inflated and gently withdrawn
o Witnessed FB aspiration o Drawing the FB with it
o With radiographic evidence of Progress is typically monitored fluoroscopically
FB Only experienced personnel should perform
o With previously described this procedure
classic signs and symptoms of Bougienage method
FB aspiration Blunt esophageal FB may be advanced into the
o Repeat bronchoscopy stomach with a bougie
After FB extraction Child is sitting upright
Inspect mucosa Lubricated instrument is gently passed down
Aspirate trapped secretions the esophagus, dislodging the object
Search multiple objects and fragments Object is then expected to pass through the
Esophageal FB rest of the GI tract
o Do not always mandate early surgical intervention Observation and a repeat radiograph
o Observation
Spontaneous passage (up to 24h)
o To rule out retained FB and Esophageal stricture/obstruction
other complications Retropharyngeal abscess
Only experienced personnel should perform Failure to thrive
this procedure Disposable diapers
Should not be performed on children with o Eliminated safety pins
known lower GI tract abnormalities Sx mimic manifestations of infection Page |
o Drugs (adult patients) o Check for systemic manifestations of infection in the hx and PE
Relax the LES Fruits with small seeds, balut, meat chunks 140
Glucagon o Given with caution to high-risk patients
Benzodiazepines Heimlichs maneuver, Back blows, Abdominal thrusts
Nifedipine
Laxatives
To hasten the passage
VI. PROGNOSIS/PREVENTION/PROPHYLAXIS
Complications :
o mostly result from a delay in diagnosis
o Airway FB
Pneumonia and atelectasis
Most common complications secondary to and
after removal of bronchial FB
Bleeding
From granulation tissue surrounding the FB or
erosion into a major vessel
Pneumothorax and pneumomediastinum
Can result from an airway tear
o Esophageal FB
Perforation
rare
may lead to:
o Mediastinitis
o Pneumothorax
o Pneumomediastinum
o Aortoesophageal Fistula
Formation
o Tracheal Compression
Mucosal abrasion
