UT Trauma Handbook
UT Trauma Handbook
UT Trauma Handbook
Elvis Presley Memorial Trauma Center Department of Surgery Division of Trauma and Surgical Critical Care University of Tennessee Health Science Center Memphis, Tennessee
Contents
GENERAL POLICIES Trauma Service Policies Conferences and Clinics Service Assignments and Transfer Universal Precautions in the Trauma Rooms Criteria for Triage to Trauma Rooms Routine Trauma Labs Consults HEAD/SPINE Cervical Spine Clearance Spinal Cord Injury with Deficit Dermatomes Sensory Levels Classification of Spinal Cord Injury NECK Blunt Cerebrovascular Injury Penetrating Neck Injuries CHEST Blunt Aortic Injury Emergent Thoracotomy Hemothorax ABDOMEN/PELVIS Hemodynamically Unstable Blunt Abdominal Trauma Hemodynamically Stable Blunt Abdominal Trauma Antibiotics for Penetrating Abdominal Trauma Anterior Abdominal Stab Wounds Blunt Liver Injury Blunt Splenic Injury Pancreatic Injury Organ Injury Scales Management of Pelvic Fractures Tile Classification of Pelvic Fractures VASCULAR Ligate vs. Repair Neurovascular Injuries EXTREMITIES Fracture/Dislocations Muscles and Nerves Mangled Extremity Severity Score SURGICAL CRITICAL CARE Diagnosis & Empiric Therapy of VAP Risk Factors & Prophylaxis for DVT Herbal Supplements Ventilator Weaning Management of Hypertension Pharmacologic Agents Alcohol Withdrawal Sedation Stress Ulcer Prophylaxis ICP Management 4 10 11 12 13 14 15 16 17 18 19 20 22 23 24 25 26 27 28 29 30 31 32 33 34 37 38 39 40 41 42 43 44 47 48 52 53 54 55 56 58 59
Mechanism of Injury (assumes physiological stability) Strangulations/hangings GSW/SGW of head, neck, torso Penetrating injuries of extremities with neurovascular deficit Stab wounds of head, neck, torso Steering wheel/windshield deformity Fatality within the vehicle Rollovers/ejection from vehicle Pregnant patients when history is suggestive of major trauma Intoxicated patients when history is suggestive of major trauma Blunt trauma with complaints relative to abdomen or thorax Extrication time > 20 minutes Intrusion of space > one foot Falls > 15 feet Pedestrian struck Motorcycle crash
Anatomical Alterations
Airway obstruction Pelvic instability Significant bleeding Crush (major) injury CSF leak Flail chest Open long bone fracture Depressed skull fracture/scalp avulsion Maxillofacial trauma, severe Spinal cord injuries Subcutaneous emphysema, massive Tension pneumothorax Major amputations (not fingers/toes) Multiple long bone deformities
13
14
Altered mental status, or multiple system injury, or awake with cervical pain or tenderness, or clinical signs of spinal cord injury
Poorly visualized area or abnormal C-spine cleared (document on chart), remove collar CT scan C-spine
Normal
Abnormal
Leave collar on and consult Orthopedics (admission date an odd day) or Neurosurgery (admission date an even day) for evaluation
16
Bolus methylprednisolone (Solumedrol) 30 mg/kg over 15 min (if within 8 hours from injury)
Continuous infusion 5.4mg/kg/hr for 23-47 hours* 23 hours if started 0-4 hours after injury 47 hours if started 4-8 hours after injury
Strict log roll Take off backboard Keep in cervical collar if cervical injury or altered sensorium
17
Dermatomes
18
Sensory Levels
19
MOTOR
Elbow flexors Wrist extensors Elbow extensors Finger flexors (distal phalanx of middle finger) Finger abductors (little finger)
0 = total paralysis 1 = palpable or visible contraction 2 = active movement, gravity eliminated 3 = active movement, against gravity 4 = active movement, against some resistance 5 = active movement, against full resistance NT = Not testable Hip flexors Knee extensors Ankle dorsiflexors Long toe extensors Ankle plantar flexors Voluntary anal contraction (Yes/No)
+
50
=
100
MOTOR SCORE
NEUROLOGICAL LEVELS
The most caudal segment with normal function
COMPLETE OR INCOMPLETE?
Incomplete = Any sensory or motor function in S4-S5
SENSORY MOTOR
20
SENSORY
KEY SENSORY POINTS
Pin Prick L
TOTALS
+ 56
56 56
+ =
Maximum
SENSORY MOTOR
21
Carotid injury
Vertebral injury
Neurosurgery consult
Treatment**
Treatment**
Heparin** if no contraindication (preferred for carotid & complex vertebral injuries) Start @ 1000 units/hour NO bolus
Serial PTT, 1 value 4 hours after drip started then q8hrs Goal is 1.5-2.0 x normal
st
Repeat angiogram in 14 days and/or 6 weeks if necessary Conversion to Coumadin or antiplatelet therapy depending on pathology/clinical course for at least 6 weeks, follow up in Trauma Clinic and with Neurosurgery
22
*May benefit from diagnostic test such as plain lateral c-spine X-ray, barium swallow, bronchoscopy, or laryngoscopy
To OR
Zone I
Zone II
Zone III
unstable
stable
unstable
stable
unstable
stable
To OR
To OR
To OR
Injury
No Injury
TO OR
Observe
23
Chest CT
Positive
Negative
Appropriate sedation
Arch aortogram
Appropriate mechanism of injury includes high speed impact injuries (MVC, MCC, fall, decelerating blunt injury). *BP & HR goals: systolic BP 120 mmHg, HR <90. Obtain ECG prior to blockade therapy Medications: Esmolol: 0.5 mg/kg IV loading dose over 1 minute, then 0.05 mg/kg/min over 4 minutes, then 0.1 mg/kg/min; titrate to HR <90. Advantage: very short half life (9 minutes) Disadvantage: side effect of hypotension may require cessation of therapy Labetalol: 10-20 mg IV slowly followed by continuous IV infusion of 1-2 mg/min. Additional bolus dose of 20 mg may be given up to a total of 300 mg. Continuous infusion must be titrated to the desired endpoints. Advantage: blockade of and with single agent therapy Disadvantage: half life 5-8 hours Nitroprusside: 0.3 mcg/kg/min initial dose, then titrate to BP goal. Maximum dose is 10 mcg/kg/min. Advantage: extremely short half life Disadvantage: can increase dP/dT and cause reflex tachycardia. NEVER use without blockade therapy.
24
Emergent Thoracotomy
Mechanism of Injury
Blunt
Penetrating*
Pronounce
Cardiac ultrasound
Pronounce
Negative
Positive
Emergent thoracotomy
* Only for penetrating wounds to the upper abdomen or chest (cardiac box). Resuscitative thoracotomy for penetrating abdominal wounds without suspicion of cardiac injury is not indicated.
25
Hemothorax Management
Place Chest Tube
Remove Tube
Clot Resolved No
No
1) Residual clot > 500cc OR 2) Residual clot occupies >1/3 of thoracic cavity OR 3) Unchanged Yes Candidate for VATS? Yes No
2 1
VATS
No
Clot Resolved
Infuse TPA per chest tube q 24 hours x 3 days (check daily Chest x-ray) Daily Chest X-Rays Repeat CT Chest Yes 48 Hours Repeat CT Chest
Remove Tube
Clot Resolved No
Clot Resolved
Repeat CT Chest
VATS Contraindications 1) Coagulopathy 2) Hemodynamic instability 3) Inability to tolerate single lung ventilation
TPA Infusion Protocol 1) Obtain HCT, PT, PTT prior to infusion (if abnormal consider not using rTPA) 2) Mix 4mg of rTPA (Reteplase ) in 50cc sterile saline. 3) Instill mixture into chest tube and flush tube with 50cc of sterile saline. 4) Clamp chest tube for 4 hours (observe patient for 10 minutes for problems with breathing). 5) Mobilize patient. 6) Check HCT, PT, PTT 1 hour after infusion (if significantly changed from baseline, consider stopping infusion)
26
TPA Contraindications 1) Active bleeding OR 2) CVA in past 30 days OR 3) Intracranial hemmorhage OR 4) Intracranial Neoplasm OR 5) Coagulopathy OR 6) Pregnancy OR 7) Chest tube with air leak
F.A.S.T.
DPL
Grossly positive*
To OR
To OR
To OR
*Criteria for positive DPL: Grossly positive - >10cc blood RBC - >100,000 cells WBC - >500 cells at least 1 hour after injury
27
Physical exam
Nontender
Tender CT scan
CT scan
Normal
Abnormal2
Normal
Discharge1
1 2
If any doubt, admit the patient for at least 23 hours May require DPL or other evaluation depending on findings
28
No further antibiotics
No further dosing
*For patients with penicillin allergy, give ciprofloxacin 400 mg IV every 12 hours (2 total doses for hollow organ injury, only the preop dose for no hollow organ injury) and metronidazole 500 mg every 6 h (4 total doses for hollow organ injury, only the preop dose for no hollow organ injury)
29
Yes
No
To OR
Discharge
30
CT scan
Grades 1,2,3
Becomes unstable
Grades 4,5
Stable
Stable, improving
DC from ICU
Quantitation of hemoperitoneum
Small- perihepatic Moderate- Small + paracolic gutter Large-Moderate + pelvis Repeat CT 1 month
Outpatient management
Grade 1,2,3 Grade 4,5
healed
Not healed
Becomes unstable
Age < 50
Angioembolization
Grade 3-5
OR
Grade 1 Floor
Large hemoperitoneum
F/U CT 24 hours
Worse
OR
ICU*
Quantitation of hemoperitoneum:
Small perihepatic/splenic Moderate small + paracolic gutter Large moderate + pelvis
Floor
Stable
Consider splenectomy
OR
Outpatient Management
Grade 1,2 Grade 3-5
CT if clinically indicated
Healed
CT in 1 month
Not healed
Activity ad lib
32
Pancreatic Injury
Duct injury
No
Indeterminate
Yes
Drain
Low probability
High probability
Resection + drainage
High probability of ductal injury: - direct ductal visualization - complete pancreatic transection - >50% pancreatic laceration - severe maceration - pancreatic fluid leak
33
Description of injury
Subcapsular, <10% surface area Capsular tear, <1cm parenchymal depth Subcapsular, 10%-50% surface area; intraparenchymal, <5 cm in diameter Capsular tear, 1-3cm parenchymal depth that does not involve a trabecular vessel Subcapsular, >50% surface area or expanding; ruptured subcapsular or parecymal hematoma; intraparenchymal hematoma > 5 cm or expanding >3 cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels producing major devascularization (>25% of spleen) Completely shattered spleen Hilar vascular injury with devascularizes spleen
34
Description of injury
Subcapsular, <10% surface area Capsular tear, <1cm parenchymal depth Subcapsular, 10% to 50% surface area: intraparenchymal <10 cm in diameter Capsular tear 1-3 parenchymal depth, <10 cm in length Subcapsular, >50% surface area of ruptured subcapsular or parenchymal hematoma; intraparenchymal hematoma > 10 cm or expanding 3 cm parenchymal depth Parenchymal disruption involving 25% to 75% hepatic lobe or 1-3 Couinauds segments Parenchymal disruption involving >75% of hepatic lobe or >3 Couinauds segments within a single lobe Juxtahepatic venous injuries; ie, retrohepatic vena cava/central major hepatic veins Hepatic avulsion
35
Description of injury
Microscopic or gross hematuria, urologic studies normal Subcapsular, nonexpanding without parenchymal laceration Nonexpanding perirenal hematoma confirmed to renal retroperitoneum <1.0 cm parenchymal depth of renal cortex without urinary extravagation >1.0 cm parenchymal depth of renal cortex without collecting system rupture or urinary extravagation Parenchymal laceration exteding through renal cortex, medulla, and collecting system Completely shattered kidney Main renal artery or vein injury with contained hemorrhage Avulsion of renal hilum which devascularizes kidney
36
Open
Closed fracture
fracture
OR Supraumbilical DPL, F.A.S.T
Positive
Negative
Positive
Negative
T-pod
T-pod
T-pod
T-pod
OR
CT
Angiography
37
38
39
40
Fracture/dislocation of Extremity
Pulses equal
Pulse deficit
41
C7 C8, T1 Median
42
Limb ischemia
Pulse reduced or absent but perfusion normal Pulseless, paresthesias, diminished capillary refill Cool, paralyzed, insensate, numb 1* 2* 3*
Shock
Systolic BP always > 90 mm Transient hypotension Persistent hypotension 0 1 2
Age (years)
< 30 30-50 > 50 * Score doubled for ischemia > 6 hours 0 1 2
The MESS is the sum of scores from each category. Scores < 7 are associated with limb salvage, Scores > 10 are associated with primary amputation. Outcome is variable for scores 7-10.
43
44
Trauma ICU Ventilator-Associated Pneumonia Clinical Pathway Diagnosis and Empiric Management
Clinical Suspicion of VAP Fiberoptic Bronchoscopy with BAL Empiric antibiotic therapy based on timing of ICU admission
No growth to date
Significant (100,000)
Defined as the appearance of a new or changing infiltrate on chest radiograph and at least 2 of the following: o o Abnormal temperature (>38 C or <36 C); 3 3 Abnormal white blood cell count (>10,000 cells/mm or <4000 cells/mm or the presence of >10% immature bands); Macroscopically purulent sputum -If severe beta-lactam allergy, change: Unasyn to Levofloxacin 750 mg IV Q24H, Cefepime to Ciprofloxacin 400 mg IV Q8H; dosage adjustment may be necessary based on renal function **Continue to monitor for changes in Final culture results
45
Yes
No
Discontinue Antibiotics
* Adequate antibiotic therapy is antibiotic therapy with in vitro activity against the pathogen. Patients extubated or not eligible for repeat BAL should be treated for 7 full days (consider 10-14 days if Pseudomonas or not responding clinically) ** Consider treatment for 10,000 cfu/mL in severely injured patients with Pseudomonas and/or Acinetobacter Use final culture result. Continue antimicrobial therapy in patients with septic shock Pseudomonas requires a follow-up BAL regardless of being early or late VAP
46
Guideline for the Prevention of Venous Thromboembolism in Critically ill Patients Approved by Pharmacy and Therapeutics Committee May 2004
Baseline CBC, BMP, PTT, and PT/INR
examples include: Traumatic brain injury with progression on head Active hemorrhage CT >24h post-injury (consult neurosurgery) Recent hemorrhagic stroke Hx of Heparin-induced Thrombocytopenia (HIT) INR > 1.6 Epidural catheter present (consult anesthesia) PTT > 60 sec 9 Platelet count < 50 x 10 cells/L No
Yes
Sequential compression devices (preferred) or A-V foot pumps. Consider serial duplex ultrasound in high-risk patients
Spinal cord injury Spinal column fractures Long bone fracture Pelvic fracture Sacral fracture
Acetabulum fracture Traumatic brain injury Laparotomy Age > 40 plus major surgery, cancer, history of
No
Unfractionated heparin 5,000 * units sq every 8 hours plus Sequential compression devices (preferred) or A-V foot pumps *Note: May not be indicated in burn patients unless other risk factors are present.
Yes
N o
Enoxaparin 30mg sq every 12 hours plus Sequential compression devices (preferred) or A-V foot pumps
Unfractionated heparin 5,000 units sq every 8 hours plus Sequential compression devices (preferred) or A-V foot pumps
Enoxaparin 30mg sq every 12 hours plus Sequential compression devices (preferred) or A-V foot pumps
Reevaluate all patients for continuation of venous thromboembolism prophylaxis upon ICU discharge
[A] Consider Inferior Vena Cava (IVC) filter in: High-risk trauma patients with significant bleeding risk or Patients with injury pattern rendering them immobile for prolonged period of time: a) Severe Traumatic brain injury b) Spinal cord injury with para- or quadriplegia c) Complex pelvic fracture with associated long bone fracture(s) d) Multiple long bone fractures
Evidence-based references Geerts WH, et al. Chest 2001; 119: 132S-175S. Available at http://www.chestjournal.org/cgi/reprint/119/1_suppl/132S (accessed 5/14/04) Rogers FB, et al. J Trauma 2002; 53(1):142-164. Also available at http://www.east.org/tpg/dvt.pdf (accessed 5/14/04) Modified 5/14/04
47
Effect
Ingredient(s) Responsible
Coumarin consitiuents
Comments
There is some evidence that the related Angelica species can inhibit platelet aggregation and lower prothrombin time when combined with warfarin. The coumarin constituents of related Angelica species can inhibit human platelet aggregation in vitro. The related species, Angelica sinensis, can lower prothrombin time in rabbits when coadministered with warfarin. Anticoagulant effects have been seen with excessive doses of anise. (Typical dose is 0.5-1 gram of the dried leaf or 50-200 mL of the essential oil.) Theoretically, excessive use of anise might prolong coagulation, increasing PT/INR and test results, due to coumarins contained in anise. Anticoagulant effects have been noted in vivo. Dong quai can potentiate the therapeutic and adverse effects of warfarin and antiplatelet drugs. The antithrombin activity of fish oil is due to prostacyclin synthesis, vasodilation, reduced platelet counts and adhesiveness, and prolonged bleeding time. The isolated fraction, fucoidin, has 4050% of the blood anticoagulant activity of heparin, and fucus can increase the risk of bleeding.
Anticoagulant
Coumarin constituents
Asafoetida (Ferula assafoetida, assant, devils dung, fum, giant fennel) Dong Quai (Angelica sinensis, Chinese angelica, Danggui) Fish Oils (omega-3 fatty acids)
Coumarin constituents Coumarin constituents Docosahexaenoic acid (DHA) Eicosapentaenoic acid (EPA) Fucoidin
Anticoagulant
48
Effect
Coagulant Anticoagulant Antiplatelet
Ingredient(s) Responsible
Vitamin K constituent Coumarin constituents Salicin
Comments
Excessive doses of agrimony could interfere with anticoagulant therapy. (Typical dose is 3 grams/day.) Arnica could potentiate the effects of anticoagulant and antiplatelet drugs. Salicin is a salicylate constituent. However, in vitro studies provide preliminary data that suggest salicin might not potentiate the effects of anticoagulant drugs. There is insufficient reliable information to determine if there is enough salicylate present in black cohosh to have significant effects. Excessive doses of bogbean can increase the risk of bleeding due to the hemolytic effects of an unknown constituent. (Typical dose is 1-2 mL of the 1:1 liquid extract in 25% alcohol TID or 1-3 grams of the dried leaf TID.) Excessive doses could increase the risk of bleeding. (Typical dose is 60-200 mg of the dried leaf TID.) Borage seed oil could prolong bleeding time. Bromelain could increase the risk of bleeding when used in combination with antiplatelets or anticoagulants. Capsicum has led to increased fibrinolytic activity and could prolong bleeding time. Celery could have anticoagulant effects due to the apiogenin constituent. Clove contains a volatile oil that consists primarily of eugenol. There is one case report of increased international normalization ratio (INR) with concomitant use of danshen and warfarin. Studies show that lectin can have agglutinating activity and could interfere with anticoagulant or coagulant therapy. Fenugreek could potentiate the effects of anticoagulant and antiplatelet drugs. The crude extracts can inhibit platelet aggregation and the neutrophil and platelet secretory activity. This could potentiate the effects of anticoagulant and antiplatelet drugs. Panax ginseng could decrease the effectiveness of warfarin and affect clotting time. Goldenseal could inhibit the anticoagulant effects of heparin. Aesculin may increase bleeding time due to antithrombin activity, which could increase the risk of bleeding when used concomitantly with anticoagulants or antiplatelets.
Black cohosh (Cimicifuga racemosa, baneberry, black snakeroot, bugwort) Bogbean (Menyanthes trifoliata, buckbean, marsh trefoil, water shamrock)
Antiplatelet
Salicylate
Bleeding risk
Unidentified constituent
Boldo (Peumus boldus, boldine) Borage Seed Oil (Borago officinalis, burage, starflower) Bromelain (Ananas comosus, bromelin) Capsicum (Capsicum frutescen, African pepper, cayenne, chili pepper) Celery (Apium graveolens, smallage, Apii fructus) Clove (Syzygium aromaticum, caryophyllus) Danshen (Salvia miltiorrhiza, red sage, salvia root) European Mistletoe (Viscum album, all-heal, devils fuge, drudenfuss) Fenugreek (Trigonella foenum-graecum, birds foot, Greek hay) Feverfew (Tanacetum parthenium, featherfew, midsummer daisy, bachelors button) Ginseng, Panax (Asian ginseng, Korean red, jintsam) Goldenseal (Hydrastis canadensis, yellow puccoon, eye balm) Horse Chestnut (Aesculus hippocastanum, escine, venostat)
Enzyme constituent Capsaicinoid constituents Apiogenin (coumarin) Eugenol Protocatechualdehyde 3,4-dihydroxyphenyllactic acid Lectin Coumarin constituents Crude extracts
49
Horseradish (Armoracia rusticana, pepperrot, mountain radish) Licorice (Glycyrrhiza glabra, sweet root) Meadowseet (Filipendula ulmaria, bridewort, dropwort) Northern Prickly Ash (Zanthoxylum americanum, toothache bark, pepper wood) Onion (Allium cepa)
Anticoagulant
Coumarin constituents
Antiplatelet Anticoagulant
Anticoagulant
Coumarin constituents
Peroxidase stimulates the synthesis of arachidonic acid metabolites, which could potentiate the anticoagulant activity of other drugs or natural products. Licorice has shown antiplatelet activity in vitro. There is insufficient reliable information to know if the side effects and toxicity normally associated with salicylates could occur. Excessive ingestion of northern pickly ash might potentiate anticoagulant therapy. Inhibits platelet aggregation in humans and could increase the risks of bleeding with antiplatelet drugs or natural products. There is one case report of increased INR associated with the use of warfarin and papaya extract. Excessive doses of passionflower could increase the risk of bleeding. (Typical dose is 0.5-1 mL of the 1:1 liquid extract in 25% alchohol TID or 0.25-2 grams of the dried plant.) Pau darco may potentiate the effects of anticoagulants and increase bleeding tendency. Excessive doses of plantain could interfere with anticoagulant therapy. (Typical dose is 2-4 mL of the 1:1 liquid extract in 25% alcohol TID or 2-4 grams of the dried leaf TID.) Salicin is a salicylate constituent. However, in vitro studies provide preliminary data that salicin might not potentiate the effects of anticoagulant drugs. Excessive doses of quassia could increase the risk of bleeding. Large amounts of red clover can increase the effects and bleeding risk of anticoagulant drugs or natural products. Large amounts of Roman chamomile could have anticoagulant effects. Large amounts of safflower could potentiate the risk of bleeding with anticoagulant drugs or natural products. Excessive ingestion of southern pickly ash might potentiate anticoagulant therapy. (Typical dose is 3-4 mL of the 1:1 liquid extract in 25% alcohol TID.) Multiple cases of decreased INR have been reported, although none have involved thromboembolic complications. Excessive doses of stinging nettle could interfere with anticoagulant therapy. Large amounts of sweet clover could potentiate the risk of bleeding with anticoagulant drugs or natural products. Large amounts of sweet vernal grass could potentiate the risk of bleeding with anticoagulant drugs or natural products. Tonka bean can contain up to 10%
Antiplatelet
Papain (Carica papaya) Passionflower (Passiflora incarnata, Maypop, apricot vine) Pau DArco (Tabebuia impetiginosa, taheebo tea, ipes, lapacho) Plantain (Plantago major, common plantain, greater plantain) Poplar (Populus tacamahacca, balm of Gilead) (Quassia amara, bitterwood) Red Clover (Trifolium pratense, cow clover, trefoil, beebread) Roman chamomile (Chamaemelum nobile, English chamomile, garden chamomile, whig plant) Safflower (Carthamus tinctorius, saffron, zaffer) Southern Prickly Ash (Zanthoxylum clava-herculis, sea ash, yellow wood) St. Johns Wort Stinging Nettle (Urtica dioica, nettle) Sweet Clover (Melilotus officinalis, common melilot, hay flower, sweet lucerne) Sweet Vernal Grass (Anthoxanthum odoratum, spring grass) Tonka Bean (Dipterux
Anticoagulant Coagulant
Lapachol Vitamin K
Antiplatelet
Salicin
Anticoagulant Anticoagulant
Coagulant Coagulant Anticoagulant Anticoagulant Anticoagulant Vitamin K Dicumarol Coumarin constituent Coumarin constituent
50
odorata, coumarouna, torquin bean) Turmeric (Curcuma longa, tumeric, Indian saffron) Wild Carrot (Daucus carota, Queen Annes lace, beesnest plant) Wild Lettuce (Lactuca virosa, green endive, lettuce opium) Willow Bark (Salix alba, white willow, silberweide) Yarrow (Achillea millefolium, thousand-leaf, wound wort) Antiplatelet Curcumin
Coagulant
Achilleine
coumarin and theoretically potentiate the risk of bleeding associated with anticoagulant drugs or natural products. Curcumin has anti-inflammatory activity and could potentiate the antiplatelet activity of other drugs or natural products. Large amounts of wild carrot could potentiate the risk of bleeding with anticoagulant drugs or natural products. Large amounts of wild lettuce could potentiate the risk of bleeding with anticoagulant drugs or natural products. Data suggests irreversible inhibition of thrombocytes is unlikely and there might be no increase interaction with blood coagulants. There is some evidence to suggest that achilleine has decreased clotting time.
HERBS WITH ANTICOAGULANT/ANTIPLATELET POTENTIAL: Concomitant use of herbs that have coumarin constituents or affect platelet aggregation could theoretically increase the risk of bleeding in some people. These herbs include anise, arnica, asafoetida, bogbean, boldo, capsicum, celery, chamomile, clove, danshen, fenugreek, feverfew, garlic, ginger, ginkgo, Panax ginseng, horse chestnut, horseradish, licorice, meadowsweet, prickly ash, onion, papain, passionflower, poplar, quassia, red clover, turmeric, wild carrot, wild lettuce, willow, and others.
51
No
Yes
No
Yes
52
MANAGEMENT OF HYPERTENSION Diagnosis of Hypertensive Crisis Immediate control to minimize end organ damage (CNS - hypertensive encephalopathy; cardiac - AMI, BAI, dissecting aortic aneurysm; renal ARF) is necessary. Otherwise BP should be lowered slowly and cautiously. Management of Hypertension There are many causes of hypertension in ICU patients, common causes include: - underlying hypertension - cold, shivering - agitation - hypoxia, hypercarbia - pain - increased ICP - withdrawal - transducer height etc. Treat underlying causes prior to administration of antihypertensives Common intravenous antihypertensive agents:
Drug
Metoprolol
Action
-1 antagonist (min -2 antagonist) -1 antagonist (mod -2 antagonist) -1 antagonist -1 antagonist (min -2 antagonist) Exogenous source of nitric oxide Exogenous source of nitric oxide Direct arterial smooth muscle relaxation ACE Inhibition
Effect
Negative chronotropy Negative inotropy Negative chronotropy Negative inotropy Vasodilation
Dose
IVP: 2.5 to 15 mg slow IVP every 6 hours IVP: 5 to 20 mg slow IVP every 1 to 4 hours Bolus: 5-20 mg IVP Infusion: 0.5 to 4 mg/min (Titrate) Bolus: 250-500 mcg/kg slow IVP Infusion: 25-100 mcg/kg/min (Titrate) Infusion: 5 to 20 mcg/min (Titrate; max 400 mcg/min) Infusion: 0.1 to 10 mcg/kg/min (Start low and Titrate) IVP: 5 to 20 mg slow IVP every 4 to 6 hours IVP: 0.625 to 1.25 slow IVP every 6 hours
Comments
Half-life 4 to 6 hours Oral:IV conversion 2.5:1 No vasodilation Half-life 4 to 6 hours Monitor closely in asthmatic patient (beta2 antagonist) Half-life ~ 15 min No vasodilation Methemoglobinemia Headache Profound hypotension Cyanide toxicity Reflex tachycardia Intrapatient variability Reflex tachycardia Hyperkalemia Acute renal failure Angioedema
Labetalol
Esmolol
Negative chronotropy Negative inotropy Venous vasodilation (min arterial dilation) Arterial and venous vasodilation Arterial dilation Vasodilation (arterial > venous)
Nitroglycerin
Nitroprusside
Hydralazine
Enalapril
Oral antihypertensives can be used in patients with stable hemodynamics. Otherwise use of IV antihypertensives is more easily titratable in ICU patients. Note on choice of antihypertensives: avoid -blockers in patients with increased adrenergic activity (pheochromocytoma, use of sympathomimetic drugs such as cocaine, amphetamine etc) avoid -blockers in patients with poor LV function, also check for other contraindications (bronchospasm) nimodipine produces cerebral vasodilation, effect noticeable in areas of brain with restricted circulation than healthy areas, usually used in patients with vasopasm after subarachnoid hemorrhage nitrates and nitroprusside can produce cerebral vasodilation and hence should be avoided in patients with intracranial pathology prolonged nitroprusside administration can lead to acidosis and cyanide toxicity
53
1
Mechanically ventilated trauma patient requiring sedation
YES
3 2
Patient w/TBI, ICP, or requiring frequent neurologic examinations?
YES
Preferred - Propofol (Diprivan brand) continuous infusion1 PLUS Morphine sulfate prn pain/agitation 2 OR Alternative - Fentanyl continuous infusion 2 Titrate to Riker SAS of 4 May consider use of neuromuscular blocker to assist with ventilator compliance 7 Lorazepam prn agitation, THEN Lorazepam continuous infusion if dosing requirements are high 4 PLUS Morphine sulfate prn pain/agitation, THEN Morphine sulfate continuous infusion if dosing requirements are high2 Titrate to Riker SAS of 4 In refractory cases, may use Propofol (generic) continuous infusion1 PLUS Morphine sulfate prn pain/agitation2
REASSESS Pt every shift & as needed
4
Patient w/TBI, ICP, or requiring frequent neurologic examinations? NO
NO
5 Go to 12 YE S
6
Pt expected to require sedation for 24 hours?
YES
NO
8
Pt requiring sedation after 24 hours?
9
Preferred Midazolam prn agitation3 PLUS Morphine sulfate prn pain/agitation2 Alternative - Propofol (generic) continuous infusion1 PLUS Morphine sulfate prn pain/agitation2
10
Continued need for sedation past 24 hours? NO
YES
NO 11
Go to 12
12
D/C Sedation Protocol, continue Morphine sulfate prn pain (or morphine sulfate 2 continuous infusion)
57
PANCURONIUM Half-life: 2 hours. May cause tachycardia. Titrate to 2/4 TOF. Dosage (continuous
infusion): 0.06-0.1 mg/kg/h. Cost: $1.79/10 mg. 24-hour cost: ~$28.00/day.
VECURONIUM Half-life: 1.5 hours. Clearance adversely affected by renal failure. Titrate to 2/4 TOF.
Dosage (continuous infusion): 0.01 mg/kg/h. Cost: $12.39/10 mg. 24-hour cost: ~$20.00/day.
MIDAZOLAM Short acting benzodiazepine. Duration of action: 2 hours. Excellent amnestic effect. Use
with caution in elderly; may cause hypotension/respiratory depression. Contraindicated in hepatic failure. Dosage (continuous infusion): 2 mg/h. Cost: $9.48/5 mg. 24-hour cost: ~$90.00/day.
LORAZEPAM Intermediate acting benzodiazepine. Duration of action: 8-20 hours. May cause
paradoxical reactions in the elderly. Prolonged use can lead to prolonged sedation. Dosage (continuous infusion): 1 mg/h. Cost: $15.89/40 mg. 24-hour cost: ~$8.00/day.
HALOPERIDOL Butyrophenone/antipsychotic. Does not cause sedation per se; does not cause
respiratory or cardiovascular depression. Mechanism of action is to cause affective dissociation. Does have limited anticholinergic effects; may cause dystonia/tardive dyskinesia. Should use Cogentin at regularly scheduled intervals. Half-life: 18 hours. Dosage: 5-10 mg/dose. Titrate to affect up to 50 mg/dose. Cost: $0.57/5 mg. Cost per dose: $0.57-5.70.
MORPHINE Opiate, the gold standard analgesic in the ICU setting. Has sedative as well as analgesic
properties. Metabolites accumulate in renal failure. Duration of action: 4-5 hours. Causes respiratory depression, histamine release, and hypotension. Dosage (continuous infusion): 2-4 mg/h. Cost: $5.76/100 mg. 24-hour cost: $3.00-6.00/day.
FENTANYL Short acting opiate. Duration of action: 1-2 hours. Sedative and analgesic effects. Causes
respiratory depression. Does not have histamine release. Much more stable than morphine from cardiovascular standpoint. Dosage (continuous infusion): 1-5 mcg/kg/min. Cost: $1.28/1000 mcg. 24-hour cost: $12.80-64.00/day.
PROPOFOL Lipid soluble, ultra-short-acting anesthetic. Prepared in lipid carrier. Duration of action: 15
minutes. Easily titratable. Lowers ICP. Should not be used in patients with hypertriglyceridemia. Exhibits three-compartment redistribution with prolonged use, leading to prolongation of action. Bolus doses may cause hypotension. Rare fatal reactions noted in children. Dosage (continuous infusion): 20-200 mcg/kg/min. Cost: $49.95/1000 mg. 24-hour cost: $100.00-1,000.00/day. ALL PATIENTS RECEIVING DIPRIVAN MUST HAVE DAILY SERUM LACTATE AND CPK CHECKED. IF EITHER RISES, STOP DIPRIVAN IMMEDIATELTY.
54
Obtain: 1. liver function panel, INR/PT 2. BMP, magnesium, phosphorus, albumin 3. Blood glucose monitoring Provide: 1. Thiamine 100mg once daily IV/IM/PO 2. Folic acid 1mg once daily PO/IV 3. Multivitamin once daily or Cernevit 5ml in minimum 500ml IVF once daily 4. Adequate hydration
Active withdrawal
Select desired therapy: Lorazepam (preferred) or ethanol drip Note: ethanol is contraindicated in patients with pancreatitis and liver disease
Lorazepam 2-4mg PO/IV/IM q 6 hrs x 4 doses, then 12mg PO/IV/IM q 6 hrs 2 8 doses (3 day prophylaxis wean). Monitor vital signs and status q 4-6 hrs.
Ethanol 5% in D5W at initial rate of 50 ml/hr. Titrate for symptoms of early withdrawal. Wean over 3 days. Monitor vital signs and status q 4-6 hrs.
Lorazepam 2-4mg IV every 1 hr until lightly sedated and symptoms resolved. Monitor vital signs and status every hour
55
Sedation Protocol
1. (Diprivan): Begin with 0.5 mg/kg/hr, increase by 0.5 mg/kg every 5-10 minutes, up to 5 mg/kg/hr. Patients receiving propofol infusion should have serum triglyceride levels monitored every 4-7 days; propofol should be discontinued if serum triglyceride levels are 300. Patients with closed head injury being followed by the neurosurgical service may receive Diprivan brand propofol because it has been shown to decrease intracranial pressure. ALL PATIENTS RECEIVING DIPRIVAN MUST HAVE DAILY SERUM LACTATE AND CPK CHECKED. IF EITHER RISES, STOP DIPRIVAN IMMEDIATELTY. 2. Morphine sulfate: Standard regimen is 1-6 mg IV every 1-2 hours prn pain/agitation; alternative regimen is continuous infusion (100 mg/ 100 mL NS): start at 2-4 mg/hr. Patients with documented allergy to morphine sulfate and/or severe hypotension with morphine sulfate administration, may use fentanyl: load with 1-2 mcg/kg, then continuous infusion (1 mg/ 50 mL) at 0.5-5 mcg/kg/hr. 3. Midazolam (Versed): Standard regimen is 2.5-5 mg IV every 1-2 hours prn sedation. 4. Lorazepam (Ativan): Standard regimen is 1-2 mg IV every 1-2 hours prn sedation; alternative regimen is continuous infusion (20 mg/ 100mL NS): start at 1-2 mg/hr. Patients with Renal Insufficiency/Failure The preferred agents are lorazepam (Ativan) and hydromorphone (Dilaudid) 0.5-1 mg IV every 1-4 hours prn pain/sedation; continuous infusion to start at 0.5 mg/hr. AVOID meperidine (Demerol) and morphine sulfate because of increased potential for accumulation of renally excreted metabolites, normeperidine and morphine-6glucuronide, respectively. Riker Sedation-Agitation Scale (SAS) 1) Unarousable: Minimal or no response to noxious stimuli, does not communicate or follow commands 2) Very sedated: 3) Sedated: Arouses to physical stimuli but does not communicate or follow commands, may not move spontaneously Difficult to arouse, awakens to verbal stimuli or gentle shaking but drifts off again, follows simple commands Calm, awakens easily, follows commands
Anxious or mildly agitated, attempting to sit up, calms down to verbal instructions Does not calm, despite frequent verbal reminding of limits; requires physical restraint, biting ET tube
7) Dangerous agitation Pulling at ET tube, trying to remove catheters, climbing over bed rail, striking at staff, thrashing side-to-side
56
No
Yes
Yes
OR
Oral Proton Pump Inhibitor i.e. Pantoprazole 40 mg every 24 hours
> 48h Mech. Ventilation OR Coagulopathy No No Prophylaxis Indicated Re-evaluate need for treatment
Yes
IV H2 BLOCKER
i.e.Ranitidine 50 mg IV every 8 hours (For Cr Cl < 50) 50 mg IV daily
Discontinue Therapy
References
1. Cook DJ , Fuller HD, Guyatt GH et al.Risk factors for gastrointestinal bleeding in critically ill patients.N Engl J Med. 1994 Feb 10;330(6):377-81. 2. Levy MJ, Seelig CB, Robinson NJ et al.Comparison of omeprazole and ranitidine for stress ulcer prophylaxis.Dig Dis Sci 1997Jun;42(6):1255-9 3. CookD, HeylandD,Griffith L,et al:Risk factors for clinically important UGIB in patients requiring mechanical ventilation. Crit Care Med 1999;27:28122817 4. Jung R, MacLaren R. Proton-pump inhibitors for stress ulcer prophylaxis in critically ill patients. Ann Pharmacother. 2002 Dec;36(12):1929-37 *Endoscopic or radiographic evidence of peptic ulcer disease in preceding 6 weeks ** Presence and persistence and severity of risk factors should be reviewed every24h This clinical practice guideline is a systematically developed algorithm intended to assist practitioner and patient decisions about appropriate health care for specific clinical circumstances. This guideline is not a fixed protocol that must be followed, but is intended for health care professionals and providers to consider. While it identifies and describes generally recommended courses of intervention, it is not presented as a substitute for the advice of a physician or other knowledgeable health care professional or provider. Individual patients may require different treatments from those specified in this particular guideline. 58
General Management Principles for Severe (GCS 3-8) and Moderate (GCS 9-12) TBI
Use very short-acting sedatives if needed, for frequent neurological exams Especially important in first 24 hours Sedation holiday for nursing neuro check unless otherwise ordered Convert field collar to Miami J until ligamentous injury can later be ruled out Insertion of intraparenchymal ICP monitor after coagulopathy (if present) corrected (Normal PTT and INR < 1.2 desireable, <1.4 occasionally still done) Avoid thrombocytopenia Serial INR (repeat 6-8 hours after injury, then every 24 hours for 48-72 hours) Rapid evacuation of mass lesions if indicated Rule out vascular injury/hypoxic or embolic mechanisms of brain injury Rule out intoxicants as contributors to neurological status Ensure adequate ventilation and oxygenation and prevent hypercarbia Elevate HOB to 30 degrees (reverse Trendelenberg if spine not cleared) Avoid hypothermia Avoid hyperglycemia and hypoglycemia (Goal Glucose 80-150) Early nutrition, enteral preferred DVT prophylaxis with TEDs and thigh-high SCDs if possible Delay subcutaneous heparin until 24-48 hours post-injury Delay Lovenox until cleared by NSR Seizure prophylaxis (Dilantin) x 7 days for EDH, SDH, IPH/contusion, depressed skull fx, penetrating injury, GCS < 10, sz within 24 hours of injury Avoid symptomatic anemia Maintain normal ICP and CPP within desired range For elevated ICP (> 20 mm Hg x > 5 minutes): Notify Neurosurgery First Tier Therapies: Ensure HOB elevated Ensure no compression from cervical collar and neck in neutral position Ensure ventriculostomy (if present) patent and functioning Sedation and analgesia with Diprivan Drip (discontinue if elevation of CPK or lactate) or Fentanyl or Morphine Drip or Intermittent Dosage Maintain Hyperosmolar Euvolemia A Catheter, Mannitol +/- Lasix, hypertonic saline boluses, serum Na and osmolarity every 6 hours No hyperosmolar agents if osmolarity > 320 Goal serum Na 145-155 usually Cerebral Perfusion Pressure Goals 50-70 mm Hg usually Neosynephrine preferred pressor if pressors needed Dopamine in low doses
59
General Management Principles for Severe (GCS 3-8) and Moderate (GCS 9-12) TBI (continued)
Second Tier Therapies: Cerebrospinal fluid drainage/Ventriculostomy Mild, temporary hyperventilation to pCO2 30-35 Intermittent paralytics Intermittent barbiturates Third Tier Therapies: Decompressive craniotomy Barbiturate coma
In general, these are used in somewhat of a step-wise progression by tier but simultaneously within tiers (and sometimes across tiers). The idea is to have standards for all but tailor the therapy to the individual patient's physiology and injury patterns. The first tier therapies are used on essentially everyone with a severe TBI. The second tier therapies may be used prior to some of the first tier therapies or never at all. The third-tier therapies may be used prior to any second tier therapies.
60