inflammation, wound healing, trauma/ICU/Burn Flashcards
phases of inflammation
injury-> exposed collagen-> plt activating factor release and tissue factor release from endothelium-> platelets bind collagen-> release growth factors (ie-ptl-derived GF PDGR)-> PMN and macrophage recruitment
role of macrophages in wound healing- what do they release
dominant role, release PDGF (plt derived GF) and cytokines (IL-1 and TNF-alpha)
Growth and activating factors in inflammation: role of the following
1) PDGF (platelet derived growth factor)
2) EGF (epidermal growth factor)
3) FGF (fibroblastic growth factor)
4) PAF (platelet-activating factor)
1) chemotactic and activates inflammatory cells (PMNs and macrophages) and activates fibroblasts-> ECM proteins and collagen. Imp for angiogenesis and epithelialization. Chemotactic for smooth muscle cells. accelerates wound healing
2, 3) Chemotactic, activates fibroblasts, angiogenesis, epithelialization
4) generated by phospholipase in endothelium (a phospholipid) which is chemotactic for inflam cells and inc adhesion mlqs
1) what are the chemotactic factors for inflammatory cells
2) for fibroblasts
3) angiogenesis factors
4) epithelialization factors
1) PDGF, IL-8, LTB-4, C5a and C3a, PAF
2) PDGF, EGF, FGF
3) PDGF, EGF, FGF, IL-8 and hypoxia
4) PDGF, EGF, FGF
1) How long do PMNs last in tissues and in blood
2) how long do platelets last
3) lymphocyte role in inflammation
1) 1-2 days in tissues, 7 days in blood
2) 7-10 days
3) involved in chronic inflammation (T cells) and Ab production (B cells)
Type 1 hypersensitivity rx:
1) role of eosinophils
2) what type of infections have increased eosinophils
3) role of basophils, where aren’t they found
4) Mast cells role
5) role of histamine
6) role of bradykinin
7) what inactivates bradykinin and where is it found
1) release major basic protien once bound to allergin-> stimulates basophils and mast cells to release histamine
2) parasitic
3) main source of histamine in blood (not in tissue)
4) main source of histamine in tissues, primary cell in type 1 hypersensitivity
5) vasodilation, tissue edema, postcapillary leakage; primary effector type in type I hypersensitivity rxs (allergic rxs)
6) peripheral vasodilation, increased permeability, pain, pulm vasoconstriction
7) Angiotensin-converting enzyme located in lung
Nitric oxide
1) what is its precursor
2) what does it activate and end effect
3) another name for it
4) what has the opposite effect of NO
1) Arginine
2) guanulate cyclase-> inc cGMP-> vascular smooth muscle dilation
3) endothelium-derived relaxing factor
4) Endothelin-> vascular smooth muscle constriction
cytokines
1) main initial cytokine resonse to injury and infection is release of
1) TNF-alpha and IL-1
cytokines
1) largest producer of TNF
2) role of TNF-alpha
3) what can high concentrations of TNF-a cause
4) largest producer of IL-1
5) effects of IL-1 and what does it synergize with
6) which cytokine causes cachexia in CA pts
7) which cytokine is responsible for fever and how?
8) how do NSAIDS reduce fever
9) role of IL-6
1) Macrophages
2) increases adhesion mlqs, procoagulant, activates neutrophils and macs-> more cytokine production and cell recruitment
3) circulatory collapse and multisystem organ failure
4) macs
5) same as TNF-alpha, synergizes with TNF-alpha
6) TNF-alpha
7) IL-1 (how alveolar macs cause fever with atelectasis), PGE2 mediated in hypothalamus
8) reduce PGE2 synthesis
9) increases hepatic acute phase proteins (CRP, amyloid A -> activate complement), decreases albumin, pre-albumin and transferrin
Interferons
1) what are they released by
2) what stimulates release
3) effect of release
1) lymphocytes
2) viral infection or other stimulants
3) activate macs, NK cells and cytotoxic T cells-> inhibit viral replication
Cell adhesion mlqs- where are they located, what they bind and type of adhesion
1) Selectins
2) Beta-2 integrins (CD11/18 molecules)
3) ICAM, VCAM, PECAM, ELAM
1) L-selectins on leukocytes bind E- (endothelial) and P-(platelet) selectins-> rolling adhesion
2) on leukocytes, bind ICAM etc-> anchoring adhesion
3) on endothelial cells, bind beta-2 integrin mlqs located on leukocytes and platelets. Also involved in transendothelial migration
Complement- what activates the following pathways and what factors are only in each one
1) classic pathway
2) alternative pathway
3) what complement factor is common to both pathways
4) what electrolyte is required for both pathways
1) (IgG or IgM) Ag-Ab complex activates. Factors C1, C2, C4
2) endotoxin, bacteria, other stimuli activate. Factors B, D and P (properdin)
3) C3
4) Mg
Complement
1) factors that are anaphylatoxins and actions
2) membrane attack complex factors and actions
3) opsonization factors and action
4) factors involved in chemotaxis for inflammatory cells
1) C3a, C4a, C5a. increase vascular permeability, bronchoconstriction and activate mast cells and basophils
2) C5b-9b-> cell lysis (usually bacteria) by creating hole in the membrane
3) C3b and C4b- targets Ag for immune response
4) C3a and C5a
Prostaglandins
1) precursor
2) LTC4, LTD4, and LTE4 actions
3) LTB4 actions
1) arachidonic precursors
2) slow-reacting substances of anaphylaxis, bronchoconstriction, vasoconstriction followed by increased permeability
3) chemotactic for inflammatory cells
Catecholamines
1) when after injury do they peak
2) where is norepinephrine released?
2) where is epinephrine released?
1) 24-48hours
2) sympathetic postganglionic neurons and adrenal medulla
3) adrenal medulla (neural response to injury)
T/F thyroid hormone plays a major role in injury/inflammation
false
neuroendocrine response to injury
afferent nerves from site of injury stimulate CRF, ACTH, ADH, growth hormone, epi and norepi release
CXC chemokines
1) what are they
2) what is their role
3) what does CXC stand for
1) IL-8 and platelet factor 4
2) chemotaxis, angiogenesis, wound healing
3) C=cysteine, X= another amino acid
1) what oxidants are generated in inflammation
2) what are cellular defenses against oxidative species
1) superoxide anion radical (NADPH oxidase), hydrogen peroxide (xanthine oxidase)
2)superoxide anion radical- defense is superoxide dismutase
hydrogen peroxide- defence is glutathione peroxidase, catalase
primary mediator of reperfusion injury
PMNs
Chronic granulomatous disease:
1) enzyme defect and result
NADPH-oxidase system enzyme defect in PMNs-> decreased superoxide radical formation-> increased infection from bacteria and fungi
stages of wound healing- cells involved, what happens during each and time frame
1) Inflammation
2) proliferation
3) remodeling
1) days 1-10. PMNs, macs. Epithelialization (1-2mm/day)
2) 5days-3wks. fibroblasts. collagen deposition, neovascularization, granulation tissue formation; type III collagen replaced with type 1
3) 3wk to 1 year. decreased vascularity. net amount of collagen unchanged despite sig production and degradation
rate of
1) epithelialization
2) peripheral nerve regeneration
1) 1-2 mm/day
2) 1mm/day
order of cell arrival in wound: PMNs, lymphoctes, macs, fibroblasts, platelets
1) platelets
2) PMNs
3) Macrophages
4) lymphocytes
5) fibroblasts
role of the following in wound healing
1) macrophages
2) fibronectin
2) fibroblasts
1) release growth factors, cytokines, etc
2) chemotactic for macs; anchors fibroblasts
3) replace fibronectin-fibrin with collagen
predominant cell type by day:
1) day 0-2
2) days 3-4
3) days 5+
1) PMNs
2) macrophages
3) fibroblasts
1) composition of the platelet plug
2) composition of provisional matrix
3) what wounds show accelerated wound healing
1) platelets and fibrin
2) platelets, fibrin and fibronectin
3) reopened wounds bc healing cells already present
Open wounds
1) most imp factor in healing open wounds
2) where does epithelium migrate from
1) epithelial integrity
2) hair follicles (#1 site), wound edges and sweat glands
- dependent on granulation tissue in wound
- unepithelialized wounds leak serum and protein and promote bacteria
closed wounds
1)most imp factor in healing
tensile strength- depends on collagen eposition and cross-linking of collagen
1) which layer of bowel provides the strength
2) what is weakest time point for small bowel anastamosis
1) submucosa
2) 3-5days
myofibroblasts- what are they, how do they communicate and what part of wound healing are they involved in
smooth muscle cell fibroblast. communicate by gap junction. Involved in wound contraction and healing by secondary intention.
t/F: perineum has better wound contraction than leg
true
which type of collagen is:
1) MC type, found in skin, bone and tendons. Primary collagen in healed wound
2) widepread, particularly found in cornea
3) increased in healing wound, also in blood vessels and skin
4) basement membranes
5) cartilage
1) type I
2) type V
3) type III
4) type IV
4) type II
1) what aa improves wound tensile strength
2) which of the following are not required for hydroxylation and subsequent cross-linking of proline residues: Alpha-ketoglutarate, Magnesium, Vitamin C, Oxygen and Iron
1) proline cross-linking. collagen has proline every 3rd aa.
2) Magnesium
cause of scurvy
Vit C deficiency
1) max tensile strength of healed wound compared to pre-wound skin
2) what is predominant collagen over days 1-2
3) collagen over days 3-4
4) at what point has all of the type of collagen in #2 been replaced by the collagen in #3
5) when does wound reach max tensile strength
6) what inhibits collagen cross-linking
1) 80%
2) III
3) I
4) 3 weeks
5) 8 weeks
6) d-Penicillamine
optimal wound healing
1) is dry or moist environment better
2) how to inc O2 delivery
3) effect of edema
4) which vitamin counteracts the effects of steroids on wound healing
5) what amount of bacteria impedes wound healing and why
6) what drugs impair wound healing in 1st 14d after injury
1) moist
2) optimize fluids, no smoking, pain control, supp O2, arterial revascularization
3) avoid it by leg elevation
4) vit A
5) >10^5 2/2 dec O2 content, collagen lysis, prolonged inflammation
6) cytotoxic drugs- 5FU, methotrexate, cyclosporin, FK-506
1) how does DM contribute to poor wound healing
2) what albumin level sig risk for poor wound healing
3) mechanism via which steroids inhibit wound healing
1) impedes early-phase inflammation response (hyperglycemia causes poor leukocyte chemotaxis)
2) dec tensile strength
Diseases associated with abnormal wound healing- name the defect
1) Osteogenesis Imperfecta
2) Ehlers-Danlos syndrome
3) Marfan’s syndrome
4) Epidermolysis bullosa and rx
5) Scurvy
6) what extraintestinal manifestation of IBD is associated with abnl wound healing
1) Type I collagen defect
2) 10 types identifies, all collagen
3) fibrillin defect (connective tissue protein)
4) excessive fibroblasts. rx- phenytoin
5) vit C def
6) Pyoderma gangrenosum
Diabetic foot ulcers
1) where they most commonly occur
2) 2/2 what?
3) cause of 90% of leg ulcers and rx
1) Charcot’s joint (2nd MTP joint) MC, also on toes
2) peripheral neuropathy (can’t feel-> pressure from walking-> ischemia)
3) venous insufficiency. rx- Unna boot (elastic wrap)
1) what are scars made of
2) when to do scar revisions
3) what pts heal with little to no scarring
1) proteoglycans, hyaluronic acid and water
2) wait 1 year to allow for maturation, may improve with age
3) infants
1) how does cartilage get nutrients and oxygen
2) does denervation effect wound healing
3) does chemo affect wound healing
1) diffusion. Doesn’t have blood vessels
2) no
3) no effect on healing after 14 days
Keloids
1) inheritance pattern
2) difference bw them and hypertrophic scars
3) rx
4) rx hypertrophic scars
5) when do hypertrophic scars occur
1) autosomal dominant, more common in dark skinned ppl
2) in keloids collagen goes beyond original scar where as hypertrophic scar collagen is confined to original scar
3) intra-lesion steroid injection, silicone, pressure garments, XRT
4) steroid injection, silicone, pressure garments
5) burns or wounds that take a long time to heal
Platelet granules:
1) what are the alpha granules and what is their role
2) dense granules
3) platelet aggregation factors
1) platelet factor 4- aggregation
beta thrombomodulin- binds thrombin
platelet derived growth factor- chemoattractant
Transforming growth factor beta (TGF-beta)- modulates above responses
2) adenosine, serotonin and Ca
3) TXA2, thrombin, platelet factor 4
Trauma deaths by time after injury
1) when does 1st peak occur and associated injuries
2) when does 2nd peak occur and associated injuries
3) when does 3rd peak occur and associated injuries
1) 0-30min- lac of heart, aorta, brain, brainstem, spinal cord. no hope to save
2) 30min-4hr-head injury (#1), hemorrhage (#2)- golden hour. pts can be saved with rapid assessment
3) days to weeks-multi system organ failure and sepsis
1) what % of trauma is blunt injury and what is most commonly injured organ
2) most commonly injured organ in penetrating injury
3) biggest predictors of survival after fall
4) what is the median lethal dose for fall (LD50)
1) 80%. Liver (although some texts say spleen)
2) small bowel (some texts say liver
3) age and body orientation
4) 4 stories
kinetic energy calculation
1/2 MV^2; M=mass, V=velocity
1) when will you see a change in BP with hemorrhage?
2) resuscitation- when to switch to blood
1) >30% blood loss
2) 2L LR then switch to blood
MC cause of
1) death after reaching ER alive
2) death long term
3) upper airway obstruction
1) head injury
2) infection
3) tongue
1) injuries from seat belts
2) best site for cutdown for venous access
3) positive DPL- what makes it +
4) what does DPL miss
5) where to do DPL if pelvic fracture
6) when might you get a false negative FAST
1) small bowel perf, lumbar spine fx, sternal fx
2) saphenous vein at ankle
3) >10cc blood, >100,000 RBCs/cc, food particles, bile, bacteria, >500WBC/cc
4) retroperitoneal bleeds, contained hematomas
5) supraumbilical
6) free fluid
1) where might pts with hypoTN and neg FAST be bleeding
2) when do you need a CT scan following blunt trauma
3) what might a CT scan miss in trauma
4) when to go to OR for laparotomy (which doesn’t require it: peritonitis, evisceration, positive DPL, uncontrolled visceral hemorrhage, free air, diaphragm injury, indeterminant FAST, intraperitoneal bladder injury, contrast extravasation from hollow viscus, specific renal/pancreas/biliary tract injuries
1) pelvic fx, chest, extremity
2) abdominal pain, need for gen anesthesia, closed head injury, intoxicants on board, paraplegia, distracting injury, hematuria, negative DPL
3) hollow viscus or diaphragm injury
4) negative FAST
1) abdominal injuries- when do you need to go to the OR
2) first step after pt with penetrating anterior abd trauma, no obv peritonitis/eviscer and local wound exploration shows fascial violation or equivocal
1) any penetrating abd injury (GSW, evisceration), local wound exploration with fascial violation or equivocal. If no fascial violation can observe
2) diagnostic laparoscopy. If peritoneal violation-> explore. if no peritoneal violation-> d/c after recovery
Abdominal compartment syndrome
1) when do you see it
2) bladder pressure
3) cause of decreased cardiac output
4) result of low Cardiac output
5) effect on ventilation/why?
6) rx
1) after massive fluid resuscitation, trauma or abdominal surgery
2) >25-30
3) IVC compression
4) visceral and renal malperfusion-> dec UOP
5) upward displacement of diaphragm affects ventilaton
6) decompressive laparotomy
1) when to use Pneumatic antishock garment
2) when to do ER thoracotomy after
a-blunt trauma
b-penetrating tauma
3) how to perform thoracotomy
4) when should pt be transfered to OR after ED thoracotomy
1) pts with SBP70mmHg, if not situation is futile
1) when do catecholamines peak after injury
2) change in ADH, ACTH and glucagon after trauma
3) type specific blood- why do ppl get reactions to it
4) What should you do for all GCS </= 8
1) 24-48 hours
2) fight or flight response-> increase ADH, etc
3) blood is nonscreened, non cross-matched so can get effects from abs to HLA minor Ag in the donated blood
4) Head CT
5) Intubate
6) ICP monitor
Epidural hematoma
1) artery injured MC
2) shape on head CT
3) clinical picture
4) when to operate
1) middle meningeal artery
2) lenticular deformity
3) LOC-> lucid interval-> sudden deterioration (vomiting, LOC, restlessness)
4) significant neurologic degeneration or significant mass effect (shift >5 mm)
subderal hematoma
1) vessel injured
2) shape on CT
3) when to go to OR
4) who gets chronic subdural hematomas
1) tearing of venous plexus (bridging veins bw dura and arachnoid)
2) crescent-shaped
3) sig neurologic degeneration or mass effect (>1cm shift)
intracerebral hematoma-
1) where does it usually occur
2) when to operate
3) type of injury with coup and countrecoup lesions
1) frontal or temporal
2) significant mass effect
3) cerebral contusion
1) treatment for traumatic intraventricular hemorrhage
2) how to dxs diffuse axonal injury, treatment and prognosis
1) ventriculostomy if causing hydrocephalus
2) MRI better than CT. Tx- supportive, craniectomy if elevated ICP, very poor prognosis
How to calculate Cerbral Perfusion Pressure (CPP)
CPP=MAP- ICP (intracranial pressure)
When to use an ICP monitor
GCS<=8, suspected inc ICP (dec ventricular size, loss of sulci, loss of cisterns) or pt with moderate to severe head injury and inability to follow clinical exam (ie- intubated pt)
1) Normal ICP
2) When to treat ICP
3) where to keep CPP
1) 10
2) >20
3) >60
How to increases Cerbral perfusion pressure? which of the following won't: sedation and paralysis lower head of bed relative hyperventilation (CO2 30-35) Mannitol Barbituate coma ventriculostomy with CSF drainage craniotomy decompression
must RAISE the head of the bed to increase CPP
1) which side is the temporal pressure increased in for a dilated pupil
2) when does peak ICP occur
3) what can be given prophylactically to prevent seizures with moderate to severe head injury
4) how to dose mannitol
5) what level to keep Na and serum Osm in head injury pts
1) same side (CNIII, oculomotor compression)
2) 48-72hr after injury
3) keppra and fosphenytoin
4) load 1g/kg, give 0.25mg/kg q4hr after that (draws fluid from brain)
5) Na 140-150. Serum Osm 295-310 (may need to use hypertonic saline)
1) What do Racoon eyes signal?
2) Battle’s sign? and what is management
3) Nerve injured in basal skull fracture
4) nerves injured in temporal skull fx
5) what kind of blows are associated with temporal skull fx
6) when to operate for skull fx
7) cause of coagulopthy in traumatic brain injury
8) most common site of fascial nerve injury
1) per-orbital ecchymosis, anterior fossa fx
2) mastoid echymossis- middle fossa fx; can injure facial nerve CNVII. rx-if acute facial nerve injury, need exploration and repair. if delayed, likely 2/2 edema and exploration not needed
3) CN VII
4) CNVII and VIII (vestibulocochlear nerve)
5) orbital or lateral skull blows
6) if signficantly depressed (>1cm), contaminated, or persistant CSF leak no responding to conservative therapy (lumbar CSF drainage)
7) release of tissue factor
8) geniculate ganglion
Spine trauma
1) Jefferson fracture- what level, cause, rx
2) Hangman’s fracture- level, cause, rx
3) odontoid fx- level, 3 types and rx
4) Facet fx/dislocation- how they occur and what else can be injured?
1) C1 burst 2/2 axial loading. Tx- rigid collar
2) C2- caused by distraction and extension. rx- traction and halo
3) C2. Type 1- above base, stable; Type 2- at base, unstable (need fusion or halo); Type 3- extends into vertebral body (needs fusion or halo)
4) Can cause cord injury; associated with hyperextension and rotation with ligamentous disruption
Thoracolumbar Spine
1) what comprises the 3 columns of the thoracolumbar spine?
2) when is thoracolumbar spine considered unstable
3) what column is affected by compression (wedge) fx?
4) what fx is unstable and rx
5) what fx is stable
1) Anterior- anterior logitudinal ligament and anterior 1/2 of vertebral body
Middle- posterior 1/2 of vertebral body and posterior logitudinal ligament
Posterior- facet joints, lamina, spinous processes, interspinous ligament
2) if >1 column disrupted
3) anterior column only, stable
4) Burst fractures (>1 column) require spinal fusion
5) Compression (wedge) fx
1) bones that are at risk for injury in upright fall
2) when in spinal injury should you get an MRI?
3) indications for emergent spinal decompression
1) calcaneous, lumbar, wrist/forearm
2) neuro defects w/o bony injury to eval for ligamentous injury
3) fracture/dislocation not reducible with distraction, open fx, soft tissue or bony compression of cord, progressive neuro dysfnc
1) most common cause of facial nerve injury in trauma
2) technique for repairing facial lacerations
3) Le Fort Classification of Facial Fractures I-III. describe. what is the rx
1) temporal bone fx
2) preserve skin and don’t trim edges
3) Le Fort I- maxillary fx straifht across (-). rx- reduce, stabilize, intramaxillary fixation (IMF) +/- circumzygomatic and orbital rim suspension wires.
Le Fort II- lateral to nasal bone, underneath eyes, diagonal toward maxilla (/ ). rx same as I
Le Fort III-lateral orbital walls (- -). rx-suspension wiring to stablize frontal bone, may need external fixation
1) what type of facial fx have a 70% CSF leak and rx of CSF leak
2) rx of nose bleeds
1) nasoethmoidal orbital fx. conservative therapy for up to 2 weeks. Can try epidural catheter to dec CSF pressure and help leak close, may need surgical closure of dura if above fail
2) anterior- packing
posterior- try balloon tamponade 1st. May need angioembolization of internal maxillary artery or ethmoidal artery
1) rx of orbital blowout fx and who needs repair
2) Tripod fx- what is it and how to repair
3) T/F: pts with maxillofacial fx are at high risk for cervical spine injuries
1) repair pts with upward gaze or diplopia with upward vision. rx- restoration of orbital floor with bone fragments or bone graft
2) Zygomatic bone fx- ORIF for cosmesis
3) True
1) what is the #1 indicator of Mandibular injury
2) how to diagnose mandibular injury
3) rx
1) malocclusion
2) fine0cut facial CT with reconstruction
3) IMF (intramaxillary fixation- metal arch bars to upper and lower dental arches for 6-8wks) or ORIF
Neck Trauma
1) 3 neck zones of injury
2) study to get in asymptomatic pt with blunt injury
3) in asymptomatic penetrating (by 3 neck zones)
4) in symptomatic blunt or penetrating injury (shock, bleeding, expanding hematoma, losing or lost airway, subq air, stridor, dysphagia, hemoptysis, neuro defect
1)ZOne I- clavical to cricoid cartilage. Zone II- Cricoid to angle of mandible. Zone III- angle of mandible to base of skull
2) neck CT
3) Zone I- (greater potential for intrathoracic great vessel injury) angiography, bronchoscopy, esophagoscopy and barium swallow. pericardial window may be indicated. May need medium sternotomy to reach lesions
ZOne II-neck exploration in OR
Zone III-angiography and laryngoscopy. May need jaw subluxatin/digastric and SCM muscle release/mastoid sinus resection to reach vascular injuries in this location
4) neck exploration in OR immediately
Esophageal injury 1) how to diagnose 2) rx of contained injuries 3) rx of non-contained injuries if: a- small injury, minimal contamination b- extensive injury or contamination 4) Approach to esophageal injuries in: a- the neck b- upper 2/3 of thoracic esophagus c- lower 1/3 of thoracic esophagus
1) hardest neck injury to find. Do esophagoscopy and esophagogram (finds 95% of injuries when combined)
2) observe
3) a-primary closure. b-if in neck- just place drain (will heal). if in chest- chest tubes to drain injury and place spit fistula in neck (eventually will need esophagectomy)
4) a-left side, b- right thoracotomy, c- left thoracotomy
Laryngeal fracture and tracheal injuries
1) sx
2) are these non-urgent, urgent or emergent?
3) rx
1) stridor, crepitus, resp compramise
2) emergent
3) secure airway in ER (usually cricothydoidotomy). then primary repair (can use strap muscle for airway support) _ tracheostomy for most to allow edema to subside and check for stricture (convert the cric to a trach)
1) rx of thyroid gland injury
2) rx of recurrent laryngeal nerve injury
3) management of shotgun injures to neck
4) of vertebral artery bleeds
5) common carotid bleeds and complication
1) control bleed and drain (NOT thyroidectomy)
2) try to repair or reimplant in cricoarytenoid muscle)
3) get angiogram and neck CT, esophagus and trach evaluation
4) embolize or ligate without any sequela
5) ligation causes stroke in 20%
Chest trauma:
1) when to go to OR for thoracotomy after CT placement
2) how quickly do you need to drain blood in hemothorax and why
3) management of unresolved hemothorax after 2 well-placed drains
1) >1500 cc after initial insertion in one side, >250cc/hr for 3 hours, >2500cc/24 hr or bleeding with instability
2)
Sucking chest wound
1) how big does it need to be to be clinically significant
2) rx
1) >2/3 diameter of trachea
2) cover wound with dressing that has tape on 3 sides to prevent tension pneumo
1) what should you think about if pt has worsening oxygenation after chest tube placement
2) T/F Bronchus injuries are more common on the right
3) dx of thracheobronchial injury
4) rx- indications for repair and how to repair (type of incision)
1) tracheobronchial injury. one of the few indications to clamp NGT
2) True
3) bronchoscopy
4) may need to mainstem intubate pt on unaggected side repair if large air leak and respirator compromise or after 2 weeks of persistent air leak.
- right thoracotomy for right mainstem, trachea and and proximal left mainstem injuries (avoids aorta)
- left thoracotomy for distal left mainstem injuries
Injuries of the diaphragm
1) where are they more common?
2) more common in blunt or penetrating trauma?
3) signs on CXR
4) type of approach for repair
1) on left
2) blunt trauma
3) air-fluid level in chest from stomach herniation
4) transabdominal if 1wk bc will have to take down adhesions in the chest. May need mesh
1) what am I: widened mediastinum, 1st or 2nd rib fx, apical capping, loss of aortopulmonary window, loss of aortic contour, left hemothorax, trachea deviation to the right
1) aortic transection
1) where is aortic transection most common
2) how good is CXR at diagnosing?
3) when should you do aortic evaluation if nl CXR
4) Dx of aortic transection
5) operative approach
6) if pt has aortic transection and + DPL twhat should be addressed first
1) ligamentum arteriosum (just distal to subclavian takeoff) is MC. also seen near ortic valve and where aorta traverses diaphragm
2) nl in 5%
3) significant mechanism (head on car crash >45 mph, fall >15ft)
4) CT angio chest
5) left thoracotomy and repair with left heart bypass of place covered stent endograft (distal transections only)
6) abdominal ex-lap first. Rx other life-threatening injuries first.
What am I?: widened mediastinum, 1st or 2nd rib fx, apical capping, loss of aortopulmonary window, loss of aortic contour, left hemothorax, trachea deviation to the right
aortic transection
Aortic transection
1) MC place for tear and other places
2) How good is CXR at detecting
3) Diagnostic study
4) operative approach
5) T/F: you can not defer treatment to treat other life-threatening injuries or positive DPL first
1) ligamentum arteriosum just distal to subclavian takeoff (MC). Also, near aortic valve where aorta traverses diaphragm
2) misses 5%, need evaluation of aorta for pts with sig mech (head on car crash >45mph or fall >15ft
3) CT angio chest
4) left thoracotomy and repair with partial L heart bypass or place a covered stent endograft (distal transections only)
5) false, you can defer for other life-threatening injuries
what operative approach should you use for the following injuries:
1) ascending aorta, innominate artery, proximal right subclavian artery, inominate vein, proximal left common carotid
2) left subclavian artery, descending aorta
3) distal right subclavian artery
1) median sternotomy
2) left thoracotomy
3) midclavicular incision with removal of medial clavical
Myocardial contusion
1) what is MC cause of death
2) MC arrhythmia seen
3) how long to monitor and when is risk highest
1) v-tach and v-fib
2) SVT
3) risk highest in 1st 24 hours, monitor for 24-48hrs
1) flail chest ddefinition and rx and biggest pulm impairment
2) T/F: aspiration produces immediate CXR findings
1) 2+ consecutive rib fx with 2+ break sites. rx- occlusive dressing taped at 3 sides. can result in underlying pulm contusion
2) false- may not be immediate
Penetrating Chest injuries
1) first imaging study in stable pts
2) penetrating “box” injuries- location and studies to do to dx injuries
3) penetrating chest wound outside box w/o pneumo or hemothorax- what to do
4) what to do if find blood on doing pericardial window?
5) when do you need to go to OR for laparoscopy or laparotomy
1) CXR (if pneumothorax or hemothorax place a chest tube)
2) borders are clavicles, xiphoid process, nipples
- do pericardial window, bronchoscopy, esophagoschopy, barium swallow
3) need chest tube if pt req intubation otherwise just follow serial CXR
4) median sternotomy to fix possible injury to heart or great vessels, place pericardial drain
5) penetrating injuries anterior-medial to midaxillary line below the nipples (may also need penetrating box injury eval)
1) traumatic causes of cardiogenic shock
2) tension pneumo: what do you see for BP, airway pressures, breath sounds, neck veins, trachea
3) cause of cardiac compromise in tension pneumo
4) pts with what type of fx are at high risk for cardiac contusion
5) what fx put pt at high risk for aortic transection
1) tension pneumo, cardiac tamponade, cardiac contusion
2) hypotension, inc airway pressures, dec breath sounds, bulging neck veins, tracheal shift
3) 2/2 ICV/SVC compression-> dec venous return
4) sternal
5) 1st and 2nd rib fx
Pelvic trauma
1) what to do with hemodynamically unstable with pelvic fx and negative DPL, CXR and not other signs of blood loss or reason for shock
2) what other structures may be injured
3) 3 types of fx, mortality and bld loss
1) stabilize pelvis (C-clamp, external fixator, sheet) and go to angio for embolization
2) genitourinary and abdominal injuries
3) Type I- crush, unstable, mortality 20-30%, blood loss >10units
Type II- verticle incision completely transecting, unstable, mortality 8-12%, blood loss 2-10u
Type III- fx in rami, etc that doesn’t transect entire pelvis. stable.
Pelvic trauma
1) can repair be delayed for other injuries
2) Intra-op management of penetrating injury pelvic hematomas
3) Intra-op management of blunt injury pelvic hematomas
1) yes
2) open (can angio)
3) leave. if expanding or unstable-> stabilize fx, pack if in OR and go to angio for embolization. remove packs after 24-48hr
Duodenal Trauma
1) MC cause of injury
2) MC area injured
3) MC rx
4) for what section is segmental resection with primary end-to-end closure not possible
5) mortality
6) MC source of morbidity
1) blunt (crash or deceleration injury)
2) 2nd portion (descending portion near ampulla of Vater)
3) 80% get debridement and primary closure
4) second portion of duodenum
5) 25%
6) fistulas
1) rx of intra-op paraduodenal hematomas and where they are located with blunt injury
2) presentation, dx and rx of paraduodenal hemotomas
1) 2+cm is significant- open for both blunt and penetrating (usually in third portion of duodenum overlying spine in blunt injury)
2) SBO 12-72 hrs after injury, UGI shows stacked coins or coiled spring appearance (make sure no contrast extravasation). rx- conservative (NGT, TPN)- cures 90% over 2-3wk (hematoma resorbed)
1) what to do if at laparotomy and duodenal injury suspected
1) Kocker maneuver (to mobilize the duodenum) and open lesser sac through omentum. Chekc for hematoma, bile, succus and fat necrosis and if you see any do formal inspection of entire duodenum
1) how to diagnoses suspected duodenal injury
1) CT abd with contrast-1st then UGI (best)
CT- bowel wall thickening, hematoma, fre air, contrast leak or retroperitoneal fluid/air. If CT worrisome but non diagnostic, can repeat CT in 8-12 hours
1) Tx of duodenal trauma
2) What to do if in 2nd portion of duodenum and can’t do primary repair->
try to get primary repair/anastamosis
- may have to divert with pyloric exclusion and gastrojejunostomy to allow healing.
- place distal feeding jejunostomy and possibly proximal draining jejunostomy tube that threads back to injury site. Place drains.
1) place jejunal serosal patch over hole (may need whipple in future), do pyloric exclusion and gastrojejunostomy, consider feeding and draining jejunostomies, leave drains
-Trauma whipple rarely if ever indicated (v high mortality)
1) when to remove drains after duodenal injury repair
1) rx of fistulas
1) when pt tol diet without increasing drainage
2) bowel rest, TPN, octreotide, conservative management for 4-6wks.
Colon trauma 1) MC type of injury 2) repair for: a- right colon b- transverse colon c-left colon d-paracolonic hematomas
1) penetrating injury
2) a and b- perform primary repair/anastomosis
c-primary repair/anastamosis, diverting ileostomy
d-both blunt and penetrating need to be opened
rectal trauma
1) MC type of injury
2) repair of high rectal injuries
3) repair of low rectal injuries (<5cm)
4) when to place diverting ileostomy
1) penetrating
2) extraperitoneal- generally not repaired bc of inaccessibility. can do serial debridement or consider diverting ileostomy
intraperitoneal- rx- repair defect, presacral drainage, consider diverting ileostomy
3) repair transanally
4) shock, gross contamination, extensive injury
Liver trauma
1) T/F- often need to do lobectomy
2) can you ligate the common hepatic artery?
3) what is the pringle maneuver? does it stop bleeding from hepatic veins?
4) when to use an atriocaval shunt?
5) management of portal triad hematoma
1) F
2) yes- gastroduodenal artery has collaterals
3) clamping portal triad. Does not stop bleeding from hepatic veins
4) for retrohepatic IVC injury. Allows for control while performing repair
5) explore
Liver trauma cont
1) ideal repair of common biled duct injury
2) repair of portal vein injury and should you ligate portal vein
3) when to use omental graft
4) should you leave drains?
1) if 50% circumference or complex injury- do choledochojejunostomy. May need intraop cholangiogram to define injury. ALSO- place drains bc 10% of duct anastamoses leak
2) if you need to transect through pancreas to get to the injury in the portal vein need to perform distal pancreatectomy. Ligation of portal vein is associated with 50% mortality
3) place in liver lac to help with bleeding and prevent bile leaks.
4) yes!
Conservative management of blunt liver injuries
1) activity level allowed for pt
2) when should you go to the OR
1) bedrest for 5 days
2) -if pt becomes unstable despite aggressive resucitation (HR>120 or SBP4u needed to keep HCT>25)
- if active blush on CT abd or pseudoaneurysm: if posterior may be better going to angiogram (but if doubt go to OR), if anterior go straight to OR
spleen injury
1) how long does it take spleen to fully heal
2) when is postsplenectomy sepsis risk greatest
3) T/F splenic salvage is associated with increased transfusions
4) when to go to the OR/when has conservative management failed
5) activity level with conservative management
6) in what pts is threshold for splenectomy much higher
7) what immunizations do you need after trauma splenectomy
1) 6 weeks
2) greatest within 2 years of splenectomy
3) true
4) -pt unstable despite aggressive fluid resucitation (HR>120 or SBP2u needed to keep HCT>25)
- if active blush on CT abd or pseudoaneurysm
5) bedrest x 5days
6) children
7) Strept pneumo (pneumococcal), H flu (Hib), meningococcal
Pancreatic Trauma
1) MC injury type
2) what type of injury can cause pancreatic duct fractures and typical orientation of fx
3) what are CT signs of injury
4) rx of pancreatic contusion
5) rx of distal pancreatic duct injury
6) rx of pancreatic head injury that is not reparable
7) how do you decide bw a whipple vs distal pancreatectomy
1) penetrating accounts fo 80%
2) bunt injury-> fx perpendicular to duct
3) edema or necrosis of peripancreatic fat
4) leave if stable, place drains if in OR
5) distal pancreatectomy (can take up to 80% of the gland)
6) place drains initially. delayed whipple or possible ERCP with stent may eventually be necessary
7) based on duct injury in relation to SMV