ncmedic309 Posted July 20, 2006 Posted July 20, 2006 Grey-Turner's Sign Named after the British Surgeon George Grey Turner Bruising and/or discoloration of the flanks caused by the retroperitoneal leak of blood from the pancreas in hemorrhagic pancreatitis, blunt abdominal trauma, and ruptured abdominal aortic aneurysm. http://www.fmed.ulaval.ca/med-18654/prive/Cours%2014.htm#1 ---------------------------------------------------------------------------------- Cullen's Sign
Connie31079 Posted July 20, 2006 Posted July 20, 2006 From thefreedictionary.com Cul·len's sign (klnz) n. An indication of intraperitoneal hemorrhage, especially in ruptured ectopic pregnancy, in which blood causes periumbilical darkening of the skin. Now, my turn....how about: Von Willebrand disease
Ace844 Posted July 21, 2006 Posted July 21, 2006 What is Von Willebrand Disease? Von Willebrand Disease (VWD) is the most common bleeding disorder that people have. In fact, it is not a single disease, but a family of related diseases. (See Types of Von Willebrand Disease.) All the different types are caused by a problem with the Von Willebrand Factor (VWF). This is a protein in blood which is necessary for proper blood coagulation, or clotting. The genes that make VWF are " turned on " in two cell types in the body: the lining cells of blood vessels (endothelial cells) and platelets. When there is not enough VWF in the blood, or when it does not work the way it should, the blood takes longer to clot. How does blood clot normally? Blood is carried throughout the body within a network of blood vessels. When tissues are injured, damage to a blood vessel may result in leakage of blood through holes in the vessel wall. The vessels can break near the surface, as in a cut. Or they can break deep inside the body, making a bruise or an internal hemorrhage. Platelets are small cells circulating in the blood. Each platelet is less than 1/10,000 of a centimetre in diameter. There are 150 to 400 billion platelets in a normal litre of blood. The platelets play an important role in stopping bleeding and beginning the repair of injured blood vessels. When a blood vessel is damaged, there are four stages in the normal formation of a clot. Stage 1: The blood vessel is damaged and the bleeding starts. Stage 2: The blood vessels constrict to slow the flow of blood to the injured area. Stage 3: Platelets stick to, and spread on, the walls of damaged blood vessels. This is called platelet adhesion. These spreading platelets release substances that activate other nearby platelets which then clump together at the site of injury to form a platelet plug. This is called platelet aggregation. Stage 4: The surface of these activated platelets then provides a surface on which blood clotting can occur. Clotting proteins circulating in the blood are activated on the surface of the platelets to form a mesh-like fibrin clot. These proteins (Factors I, II, V, VII, VIII, IX, X, XI, XII AND XIII and Von Willebrand Factor) work like dominos, in a chain reaction. This is called the coagulation cascade. (See Figure 2.) How does VWD affect the normal clotting of blood? Von Willebrand Disease affects the last two stages in the blood clotting process. In Stage 3, a person may not have enough VWF in the blood , or it may not work normally. Because of this, the VWF cannot act as a glue to hold the platelets in place at the site of the damage to the blood vessel. The platelets do not stick to the lining of the vessel. In Stage 4, the VWF carries Factor 8 (written Factor VIII) in the bloodstream. Factor VIII is one of the proteins needed to make a solid clot. When the VWF is present at low levels, so is Factor VIII. Without normal levels of Factor VIII, a solid clot takes a very long time to form. How common is Von Willebrand Disease? Doctors now think that VWD could affect as many as 1 in 100 people. Because many of these people have only very mild symptoms, only a small number of them know they have the disease. Who is affected by Von Willebrand Disease? Von Willebrand Disease affects both men and women. However, because many women with VWD have heavy menstrual bleeding and prolonged bleeding after childbirth, more women have symptoms than men. Children, too, can have VWD. They are born with it. This is because VWD is an hereditary disorder. Can VWD be passed from parents to children? Yes. If one or both of the parents have VWD, they can pass it on to their children. ( See Heredity.). Why is it called Von Willebrand Disease? It is named after the Finnish physician, Erik Von Willebrand, who first described the condition in 1925. He realized that the disease was different from hemophilia, another important bleeding disorder, which in its severe form affects almost only males. How serious is Von Willebrand Disease? It depends on the type of disease. (See Types of Von Willebrand Disease.) Fortunately, there are effective treatments for all types of VWD. What's more, some researchers are finding that " ... mild VWD could be a health benefit. " They explain it this way. VWD makes it more difficult for platelets to stick together. Because of this, people with VWD could have less chance of blood clots blocking arteries (atherosclerosis), and therefore, less chance of heart attacks and strokes. Background: Although referred to as a single disease, von Willebrand disease (VWD) is in fact a family of bleeding disorders caused by an abnormality of the von Willebrand factor (VWF). VWD is the most common hereditary bleeding disorder. First described by Erik Adolf von Willebrand in 1926, VWD is a congenital bleeding disorder characterized by a lifelong tendency toward easy bruising, frequent epistaxis, and menorrhagia. Pathophysiology: VWD is due to an abnormality, either quantitative or qualitative, of the VWF, which is a large multimeric glycoprotein that functions as the carrier protein for factor VIII (FVIII). VWF also is required for normal platelet adhesion. As such, VWF functions in both primary (involving platelet adhesion) and secondary (involving FVIII) hemostasis. In primary hemostasis, VWF attaches to platelets by its specific receptor to glycoprotein Ib on the platelet surface and acts as an adhesive bridge between the platelets and damaged subendothelium at the site of vascular injury. In secondary hemostasis, VWF protects FVIII from degradation and delivers it to the site of injury. VWF is composed of dimeric subunits that are linked by disulfide bonds to form complex multimers of low, intermediate, and high molecular weights. The small multimers function mainly as carriers for FVIII. High molecular weight multimers have higher numbers of platelet-binding sites and greater adhesive properties. Each multimeric subunit has binding sites for the receptor glycoprotein Ib on nonactivated platelets and the receptor glycoprotein IIb/IIIa on activated platelets. This facilitates both platelet adhesion and platelet aggregation, making high molecular weight multimers most important for normal platelet function. VWd types VWD can be classified into 3 main types, of which 70-80% are considered to be type 1. Type 1 VWD is characterized by a partial quantitative decrease of qualitatively normal VWF and FVIII. An individual with type 1 VWD generally has mild clinical symptoms, and this type usually is inherited as an autosomal dominant trait; however, penetrance may vary dramatically in a single family. In addition, clinical and laboratory findings may vary in the same patient on different occasions. Typically, a proportional reduction in VWF activity, VWF antigen, and FVIII exists with type 1 VWD. Of patients with VWD, 15-20% have type 2 disease. VWD type 2 is a variant of the disease with primarily qualitative defects of VWF. Type 2 VWD can be either autosomal dominant or recessive. Of the 5 known type 2 VWD subtypes (ie, 2A, 2B, 2C, 2M, 2N), type 2A VWD is by far the most common. Type 2A VWD is inherited as an autosomal dominant trait and is characterized by normal-to-reduced plasma levels of factor VIIIc (FVIIIc) and VWF. Analysis of VWF multimers reveals a relative reduction in intermediate and high molecular weight multimer complexes. The multimeric abnormalities are commonly the result of in vivo proteolytic degradation of the VWF. The ristocetin cofactor activity is greatly reduced, and the platelet VWF reveals multimeric abnormalities similar to those found in plasma. Type 2B VWD also is inherited as an autosomal dominant trait. This type is characterized by a reduction in the proportion of high molecular weight VWF multimers, while the proportion of low molecular weight fragments are increased. Patients with type 2B VWD have a hemostatic defect caused by a qualitatively abnormal VWF and intermittent thrombocytopenia. The abnormal VWF has an increased affinity for platelet glycoprotein Ib. The platelet count may fall further during pregnancy, in association with surgical procedures, or after the administration of desmopressin acetate (DDAVP). Although some investigators found DDAVP to be clinically useful in persons with type 2B VWD, studies directed at excluding the 2B variant should be completed before DDAVP is used therapeutically. Measurements of FVIIIc and VWF in plasma are variable; however, studies involving the use of titered doses of ristocetin reveal that aggregation of normal platelets is enhanced and induced by unusually small amounts of the drug. In patients with the rare type 2M VWD, laboratory results are similar to those of certain patients with type 2A VWD. Type 2M VWD is characterized by a decreased platelet-directed function that is not due to a decrease of high–molecular weight multimers. Laboratory findings show decreased VWF activity, but VWF antigen, FVIII, and multimer analysis are found to be within reference range. Type 2N VWD is also rare and is characterized by a markedly decreased affinity of VWF for FVIII, resulting in FVIII levels reduced to usually around 5% of the reference range. Other VWF laboratory parameters (ie, VWF antigen [VWF:Ag], ristocetin cofactor activity) are usually normal. The FVIII-binding defect in these patients is inherited in an autosomal recessive manner. Evaluate patients with FVIII deficiency and a bleeding disorder that is not clearly transmitted as an X-linked disorder or those who respond incompletely to hemophilia A therapy for type 2N VWD. Unfortunately, the confirmatory test for type 2N VWD is not routinely available, likely resulting in an underestimate of the true frequency of this subtype. Type 3 is the most severe form of VWD. In the homozygous patient, type 3 VWD is characterized by marked deficiencies of both VWF and FVIIIc in the plasma, the absence of VWF from both platelets and endothelial cells, and a lack of response to DDAVP. Type 3 VWD is characterized by severe clinical bleeding and is inherited as an autosomal recessive trait. Consanguinity is common in kindreds with this variant. Less severe clinical abnormalities and laboratory abnormalities may be identified in occasional heterozygotes; however, such cases are difficult to identify. Multimeric analysis of the small amount of VWF present yields variable results, in some cases revealing only small multimers. Frequency: In the US: VWD is estimated to affect fewer than 3% of the population. Internationally: Prevalence worldwide is estimated at 0.9-1.3%. Mortality/Morbidity: The morbidity in individuals with VWD is variable. Many children with VWD are asymptomatic. Some of these children have cutaneous and/or mucus membrane bleeding (eg, easy bruising, epistaxis). Menorrhagia is a common symptom in females with VWD. It occurs in more than 50% of women with VWD and may be the only clinical manifestation of the disease. The rare type 3 VWD can manifest with severe bleeding symptoms similar to severe hemophilia (eg, hemarthrosis, intramuscular bleeding). Race: No influence of ethnicity on the prevalence of VWD exists. Sex: VWD affects males and females in equal numbers. Age: VWD is a congenital bleeding disorder and can be diagnosed at any age. CLINICAL Section 3 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography History: Many children with von Willebrand disease (VWD) are asymptomatic and are diagnosed as a result of a positive family history or during routine preoperative screening (eg, prolonged bleeding time). Importantly, remember that a wide variation in clinical manifestations exists, even for members of the same family. The history may reveal the following: Increased or easy bruising Recurrent epistaxis Menorrhagia Postoperative bleeding (particularly after tonsillectomy or dental extractions) Family history of a bleeding diathesis Bleeding from wounds Gingival bleeding Postpartum bleeding Physical: The physical exam may be normal, but the following may be present: Increased bruises Mucosal bleeding Causes: VWD is caused by an inherited defect that results in a deficiency or dysfunction of von Willebrand factor (VWF). The gene for VWF is on the short arm of chromosome 12. It spans approximately 180 kilobases (kb) and is composed of 52 exons. Exons range in size from 40 base pairs (bp) to 1.4 kb. Various point mutations, insertions, and deletions at the VWF locus have been described. In some cases, VWD is believed to result from other pathologic processes; however, because of the relatively high prevalence of VWD, its concomitant occurrence with other disease states may be coincidental. Nevertheless, acquired forms of VWD can be observed in the following conditions: Wilms tumor Congenital heart disease Systemic lupus erythematosus Angiodysplasia Seizure disorders treated with valproic acid Hypothyroidism DIFFERENTIALS Section 4 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Bernard-Soulier Syndrome Hemophilia A and B Hemophilia C Other Problems to be Considered: Other platelet function abnormalities, such as Glanzmann thrombasthenia, storage pool defects, and acquired abnormal platelet function due to medication (eg, aspirin, long-term NSAID use) Quick Find Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Click for related images. Related Articles Bernard-Soulier Syndrome Hemophilia A and B Hemophilia C Continuing Education CME available for this topic. Click here to take this CME. Patient Education Skin, Hair, and Nails Center Bruises Overview Bruises Causes Bruises Symptoms Bruises Treatment WORKUP Section 5 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Lab Studies: Screening tests Complete blood count: Assess platelet number and morphology, which should be normal in most patients with von Willebrand disease (VWD) (except those with type 2B VWD). Template bleeding time: Because it is reasonably well standardized, the template bleeding time is used as a screening test for primary hemostasis. The reference range for the bleeding time in children is longer than that of adults. Results of the bleeding time are affected by many technical factors, such as the direction of the incision and the skill of the technician. Although a bleeding time outside of the reference range may suggest a defect in hemostasis, it is not diagnostic. Similarly, a bleeding time within the reference range does not exclude the presence of such a defect. While neither sensitive nor specific for VWD, template-bleeding time is outside of the reference range in about 50% of patients with type 1 VWD. Patients with VWD types 2A, 2B, 2M, and 3 often have prolonged bleeding times. The template bleeding time has largely been replaced by automatic platelet function analyzers (PFAs) such as the PFA-100. Prothrombin time (PT) is within reference range in VWD. Activated partial thromboplastin time (aPTT): Approximately 25% of patients with type 1 VWD have aPTT results outside of the reference range. These results may be caused by concurrent deficiencies of other clotting factors in addition to, or rather than, FVIII. The aPTT should be outside of the reference range in patients with severe VWD or type 2N VWD in whom circulating FVIII levels are very low. Because aPTT and the template bleeding time are insensitive tests for VWD, add von Willebrand factor (VWF) activity to the screening tests performed for patients with suspected bleeding disorders (see below). Specific assays VWF levels are variable and can be influenced by a number of factors including blood type. Individuals with type O blood have lower values of VWF levels on average, whereas those with type AB blood have higher values of VWF. Day-to-day variation in VWF levels is a normal occurrence in the same individual; therefore, a single level within reference range does not exclude the diagnosis of VWD. FVIII activity is variably decreased. VWF activity (ristocetin cofactor): Ristocetin is an antibiotic that causes VWF to bind to and, subsequently, to activate platelets. In the ristocetin cofactor assay, platelets from individuals who are healthy, standard concentrations of ristocetin, and varying quantities of patient or control plasma are used. In individuals who are healthy, platelets rapidly agglutinate in response to ristocetin; however, the presence of plasma VWF is necessary for the reaction to occur. The degree of platelet agglutination is proportional to the concentration of VWF in the plasma. Several variations of this assay have been developed. Because the result of this assay reflects the functional activity of VWF, it is usually called the VWF activity. It is variably decreased in VWD. VWF antigen: The total plasma concentration of VWF protein is measured by one of several assays. The Laurell rocket immunoelectrophoresis technique measures the amount of VWF protein in the plasma, whereas radioimmunoassays and enzyme-linked immunoabsorbent assays reflect the number of VWF-binding sites. These tests determine the total amount of VWF antigen in the plasma but do not reflect its molecular structure and, hence, may be normal in VWD variants with abnormal multimers. Therefore, VWF antigen is variably decreased. Subtype determination In multimer analysis to determine the physical structure of VWF (ie, whether high molecular weight multimers are present), plasma is electrophoresed through agarose gel. The presence or absence of high molecular weight VWF is used to classify VWD. Absence or decreased levels of high molecular weight VWF multimers is consistent with type 2 VWD. Further analysis of VWF subunits has been performed with sophisticated electrophoretic techniques, resulting in the description of many type 2 variants. Other Tests: In some laboratories, platelet VWF analysis is performed. Gene analysis also can be performed for diagnosis. TREATMENT Section 6 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Medical Care: Minor bleeding problems, such as bruising or a brief nosebleed, may not require specific treatment. For more serious bleeding, medications that can raise the von Willebrand factor (VWF) level and, thereby, limit bleeding are available. The goal of therapy is to correct the defect in platelet adhesiveness (by raising the level of effective VWF) and the defect in blood coagulation (by raising the FVIII level). In recent years, desmopressin (1-deamine-8-D-arginine vasopressin, DDAVP) has become a mainstay of therapy for most patients with mild von Willebrand disease (VWD). At appropriate doses, DDAVP causes a 2- to 5-fold increase in plasma VWF and FVIII concentrations in individuals who are healthy and patients who are responsive. DDAVP can be used to treat bleeding complications or to prepare patients with VWD for surgery. In general, a patient's responsiveness to DDAVP prior to its use for these purposes can be determined. Once determined, such responsiveness generally is consistent in patients over time and within families. In patients with serious bleeding, prompt treatment is important in order to decrease the possibility of complications. Consultations: Consult a pediatric or adult hematologist. Activity: No evidence suggests that extensive activity restrictions are necessary for most patients with mild type1 VWD. Patients with more severe forms of VWD should follow guidelines developed for patients with severe hemophilia. In/Out Patient Meds: Epsilon amino caproic acid (Amicar) Inhibition of fibrinolysis Useful in mucous membrane bleeding Dose: 100 mg/kg/dose PO q4-6h Deterrence/Prevention: Avoid medications with known antiplatelet effects. Although aspirin is rarely taken by children, over-the-counter compounds containing acetylsalicylic acid often are used by adolescents. Ibuprofen and other nonsteroidal anti-inflammatory agents are reversible cyclooxygenase inhibitors and may cause intestinal bleeding. The risks of these and other medicines with antiplatelet effects should be considered in light of the severity of the von Willebrand disease (VWD). Provide patients with VWD a list of prescription and nonprescription medications to avoid. This list should include the following: Over-the-counter medications Aspirin Ibuprofen Naproxen Antihistamines Ethanol Antiplatelet agents Dipyridamole Ticlopidine Prescription nonsteroidal anti-inflammatory compounds Antimicrobials High-dose penicillins Cephalosporins Nitrofurantoin Hydroxychloroquine Cardiovascular medications Propranolol Furosemide Calcium channel blockers Quinidine Others Caffeine Tricyclic antidepressants Phenothiazines Valproate Heparin Prognosis: Individuals with VWD have a lifelong tendency toward easy bruising, frequent epistaxis, and menorrhagia. Patient Education: Avoid medications with antiplatelet activity. Mild activity restrictions may be necessary. For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education article Bruises. MISCELLANEOUS Section 9 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Medical/Legal Pitfalls: Failure to recognize bleeding tendency prior to elective surgery Failure to recognize associated symptoms (eg, menorrhagia) Failure to inform patient and family of activity restrictions Excessive bruising suggestive of child abuse frequently instigates an evaluation to rule out a coagulopathy. Borderline abnormal lab results may mislead an investigator/caregiver and prevent recognition of actual abuse. Because von Willebrand disease (VWD) is a common disorder, its coexistence with nonaccidental trauma needs to be considered if the evidence of abuse is strong. Alternatively, the medical professional must recognize that the caregivers of a child with VWD may be falsely suspected of abuse, with obvious stressful ramifications. Special Concerns: The dose of intranasal desmopressin used in VWD is about 15 times the dose used to treat patients with diabetes insipidus. A more concentrated nasal spray (1.5 mg/mL) is available for patients with VWD compared to the spray used for individuals with diabetes insipidus (0.1 mg/mL). Restrict free-water intake to avoid hyponatremia, especially in very young or elderly patients. May repeat desmopressin at intervals of 12-24-hours; however, depletion of tissue stores eventually develops. BIBLIOGRAPHY Section 10 of 10 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography Batlle J, Torea J, Rendal E, Fernandez MF: The problem of diagnosing von Willebrand's disease. J Intern Med Suppl 1997; 740: 121-8[Medline]. Carcao MD, Blanchette VS, Dean JA, et al: The Platelet Function Analyzer (PFA-100): a novel in-vitro system for evaluation of primary haemostasis in children. Br J Haematol 1998 Apr; 101(1): 70-3[Medline]. Lee CA, Brettler DB, eds: Guidelines for the diagnosis and management of von Willebrand disease. Haemophilia 1997; 3: 1-25. Mannucci PM: Treatment of von Willebrand's Disease. N Engl J Med 2004 Aug 12; 351(7): 683-94[Medline]. Nichols WC, Ginsburg D: von Willebrand disease. Medicine (Baltimore) 1997 Jan; 76(1): 1-20[Medline]. Sadler JE: A revised classification of von Willebrand disease. For the Subcommittee on von Willebrand Factor of the Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis. Thromb Haemost 1994 Apr; 71(4): 520-5[Medline]. Werner EJ: von Willebrand disease in children and adolescents. Pediatr Clin North Am 1996 Jun; 43(3): 683-707[Medline]. Werner EJ, Abshire TC, Giroux DS, et al: Relative value of diagnostic studies for von Willebrand disease. J Pediatr 1992 Jul; analysis(1): 34-8[Medline]. Zhang Z, Blomback M, Anvret M: Understanding von Willebrand's disease from gene defects to the patients. J Intern Med Suppl 1997; 740: 115-9[Medline]. Now How about Chvostek’s and Trousseau’s Signs???
whit72 Posted July 21, 2006 Posted July 21, 2006 Chvostek's Sign Spasm produced when you tap over the facial nerve. Trousseau's Sign Not sure of this one. Here is one: Kernig's Sign
Ace844 Posted July 21, 2006 Posted July 21, 2006 Chvostek's Sign Spasm produced when you tap over the facial nerve. Trousseau's Sign Not sure of this one. Here is one: Kernig's Sign WHICH IS A SIGN AND SX OF WHAT D/O??? EXPLAIN...
AZCEP Posted July 21, 2006 Posted July 21, 2006 Come on now Whit, answer the first one before throwing out another one. Chvostek's sign is facial muscle spasm related to hypocalcemia. It is created by the increased muscle tetany from the facial nerve. Trousseau's sign, good combination by the way Ace, is a spasm of the flexor muscles of the upper arm when pressure is applied for a period of time. It is also associated with hypocalcemia, and is easily elicited by inflating the blood pressure cuff, waiting a moment, and watching the flexor response. Kernig's sign is a symptom of meningitis evidenced by reflex contraction and pain in the hamstring muscles when attempting to extend the leg after flexing the thigh upon the body. Now for something a bit more challenging. What are the vital sign changes associated with the four stages of shock?
ncmedic309 Posted July 22, 2006 Posted July 22, 2006 I just kept this simple, if someone wants to elaborate further, please do so... Vital Sign Changes in Shock 1.Initial- Changes are minimal 2. Compensation - Increased Heart Rate, BP usually remains within normal range, Increased Respiratory Rate 3. Progressive/Decompensation - Hypotension occurs along with tachycardia, getting closer to death, Respirations may initially be fast, then progressively slower 4. Refractory/Irreversible - Hypotension along with bradycardia, decrease in respirations, death Edit: Forgot to add in another topic...how about MODS (Multiple Organ Dysfunction Syndrome)?
ncmedic309 Posted July 24, 2006 Posted July 24, 2006 Ok, since nobody wants to put anything in on this one... MODS (Multiple Organ Dysfunction Syndrome) As defined in Brady's Essentials of Paramedic Care, MODS is defined as a progressive impairment of two or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury. The most common causes of MODS are sepsis and septic shock. Sepsis will initially be present and it will progress into a septic shock and then ultimately into MODS or a systemic inflammatory response syndrome. The mortality rate for MODS is 60-90%. MODS also results from diseases and injury such as: -Trauma -Burns -Surgery -Hemorrhagic and Cardiogenic Shock -Acute Pancreatitis -Acute Renal Failure Risk Factors for MODS are: -Age > 65 years -Malnutrition -Pre-existing Chronic Disease (DM and Cancer) Clinical Presentation of MODS: Within 24 hours - Low grade fever, tachycardia, dyspnea, AMS, and hypermetabolic states are present. At 24-72 hours - Pulmonary failure is present At 7-10 days - Liver failure, intestinal failure, and renal failure begins At 14-21 days - Renal and Liver failure become more significant, GI collapse, and Immune collapse occurs Past 21 days - Hematolgic and Cardiogenic failure begins, AMS secondary to encephalopathy, and death occurs Source: Brady's Essentials of Paramedic Care, 2003. Next Topic - The Cranial Nerves (Function and Assessment)
AZCEP Posted July 24, 2006 Posted July 24, 2006 I-Olfactory cribiform plate of ethmoid nasal cavity special sensory olfactory epithelium - smell -------------------------------------------------------------------------------- II-Optic optic canal of sphenoid orbit special sensory retina-vision -------------------------------------------------------------------------------- III-Oculomotor superior orbital fissure orbit somatomotor levator palpebrae superioris superior rectus medial rectus inferior rectus inferior oblique visceromotor preganglionic parasympathetic to: ciliary ganglion (innervation of sphincter pupillae and ciliary muscle) -------------------------------------------------------------------------------- IV-Trochlear superior orbital fissure orbit somatomotor superior oblique muscle (poverty muscle) -------------------------------------------------------------------------------- V1-Trigeminal opthalmic (Major branches: Lacrimal, Frontal, Nasociliary, and Meningeal branch) superior orbital fissure orbit general sensory general sensation from skin and mucosa in region at and above orbit V2-Trigeminal maxillary (Major branches: Infraorbital, Zygomatic, Nasopalatine, and Palatine branch) foramen rotundum pterygopalatine fossa general sensory general sensation from skin and mucosa in region from orbit to mouth V3-Trigeminal mandibular (Major branches: Buccal, Auriculotemporal, Lingual, Inferior Alveolar, and Meningeal branch) foramen ovale with lesser petrosal from CN9 infratemporal fossa branchiomotor muscles of mastication tensor tympani tensor veli palatini mylohyoid anterior belly digastric general sensory general sensation from the skin and mucosa from region at and below the mouth -------------------------------------------------------------------------------- VI-Abducens superior orbital fissure orbit somatomotor to lateral rectus (best abductor!) -------------------------------------------------------------------------------- VII-Facial (Major motor branches: Temporal, Zygomatic, Buccal, Mandibular, Cervical, and Posterior Auricular) internal acoustic meatus-> facial canal-> stylomastoid foramen temporal bone branchiomotor muscles of facial expression stapedius stylohyoid mylohyoid posterior belly digastric facial canal-> middle ear-> chorda tympani-> petrotympanic fissure special sensory taste, anterior 2/3 tongue facial canal-> middle ear-> chorda tympani-> petrotympanic fissure visceromotor preganglionic parasympathetic to: submandibular ganglia (innervates submandibular and sublingual glands) greater superficial petrosal-> pterygoid canal visceromotor preganglionic parasympathetic to: pterygopalatine ganglia (innervates lacrimal gland, nasal glands, and palatine glands -------------------------------------------------------------------------------- VIII-Vestibulocochlear internal auditory meatus temporal bone special sensory hearing and balance -------------------------------------------------------------------------------- IX-Glossopharyngeal jugular foramen neck branchiomotor stylopharyngeus viscerosensory pharynx, palate, carotid sinus, carotid body and posterior 1/3 tongue special sensory taste, posterior 1/3 tongue jugular formen-> tympanic branch-> tympanic caniculus-> middle ear middle ear viscerosensory middle ear and auditory tube jugular formen-> tympanic branch-> tympanic caniculus-> middle ear infratemporal fossa visceromotor parotid -------------------------------------------------------------------------------- X-Vagus jugular foramen branchiomotor pharynx and larynx general sensory auricle, external auditory meatus viscerosensory mucosa of entire larynx visceromotor preganglionic parasympathetic to abdomen & thorax -------------------------------------------------------------------------------- XI-Spinal Accessory enters by foramen magnum-> exits by jugular foramen neck branchiomotor trapezius, sternocleidomastoid -------------------------------------------------------------------------------- XII-Hypoglossal hypoglossal canal neck somatomotor all tongue muscles (these end in ‘glossus’) are innervated by CN12 except palatoglossus Or if you would like a mnemonic: On Old Olympus, Towering Top, A Finn And German Viewed Some Hops For functions: Some Say Marry Money, My Brother Says, Bad Business, Marry Money with S=Sensory M=Motor B=Both For assessment, here is a reference card that I made up a while back: Cranial Nerve Nerve assessment I(Olfactory) Identify simple odors II(Optic) Identify letters No visual field deficit III(Occulomotor) Pupillary light reflex IV(Trochlear) Eyes follow in parallel V(Trigeminal) Contraction of masseters/Mandibular deviation Normal perception from face VI(Abducent) Eyes follow in parallel VII(Facial) Normal facial movement Symmetrical eyebrows/smile VIII(Vestibulocochlear Symmetrical hearing bilaterally IX(Glossopharyngeal) Normal gag reflex X(Vagus) Equal palate/Uvular movement XI(Accessory) Equal muscle strength head turn/shoulder shrug XII(Hypoglossal) Tongue protrudes in midline How about Brown-Sequard Syndrome?
Scaramedic Posted July 25, 2006 Author Posted July 25, 2006 [align=center:10a261db92]Brown-Sequard Syndrome [/align:10a261db92] Pathophysiology: The pathophysiology of Brown-Séquard syndrome is damage or loss of ascending and descending spinal cord tracts on one side of the spinal cord. Spinal cord anatomy accounts for the clinical presentation. The motor fibers of the corticospinal tracts cross at the junction of the medulla and spinal cord. The ascending dorsal column carrying sensation of vibration and position runs ipsilateral to the roots of entry and crosses above the spinal cord in the medulla. The spinothalamic tracts convey sensations of pain, temperature, and crude touch from the contralateral side of the body. At the site of spinal cord injury (SCI), nerve roots and/or anterior horn cells also may be affected. The structural and ultrastructural changes that occur in the cord have been studied in animals and postmortem human subjects. Scattered petechial hemorrhages develop in the gray matter and enlarge and coalesce by 1 hour postinjury. Subsequent development of hemorrhagic necrosis occurs within 24-36 hours. White matter shows petechial hemorrhage at 3-4 hours. Myelinated fibers and long tracts show extensive structural damage. Frequency: In the US: The true incidence of Brown-Séquard syndrome is not known. No national database exists to record all spinal cord syndromes resulting from both traumatic and nontraumatic etiologies. The incidence of traumatic SCIs in the United States is estimated at 11,000 new cases per year, with Brown-Séquard syndrome accounting for 2-4% of the traumatic injuries. Prevalence of all SCIs in the United States is estimated to be approximately 247,000 persons. Internationally: International incidence is unknown. Mortality/Morbidity: Acute mortality rates are measured for all traumatic SCIs without differentiation according to level or completeness. The mortality rate is 5.7% during the initial hospitalization if no surgery is performed and 2.7% if surgical intervention is performed. Mortality prior to hospitalization is not known but has decreased with the advancement of emergency medical services. Long-term mortality has been studied extensively for complete and incomplete spinal cord lesions based on age at injury and neurologic level. Statistics on mortality ratios, life expectancy, and the underlying and secondary causes of death are available from the National Model Systems Database. Morbidity following any SCI, regardless of etiology, is related to common secondary medical complications. The most prevalent complication is a pressure ulcer, followed by pneumonia, urinary tract infection, deep vein thrombosis, pulmonary embolus, and postoperative infection. Race: The SCI database indicates that 70.1% of cases of Brown-Sequard syndrome occur in the white population, 19.6% occur in the African American population, 1.2% occur in the Asian population, 1.3% occur in the American Indian population, and 7.8% occur in other races. Sex: Various demographic studies have consistently shown a greater frequency of SCI in males as compared to females. This finding primarily reflects traumatic injury data and may not be reflective of frequency of nontraumatic etiologies. Age: Population-based studies reveal SCI primarily occurs in those aged 16-30 years, but the mean age has increased over the past 30 years. If other etiologies of Brown-Séquard syndrome were considered, mean age would increase further. History: Clinical history often is reflective of the etiology of Brown-Séquard syndrome. Onset of symptoms may be acute or gradually progressive. Complaints are related to hemiparesis or hemiparalysis and sensory changes, paraesthesias, or dysesthesias in the contralateral limb(s). Isolated weakness or sensory changes may be reported. Physical: Diagnosis and identification of Brown-Séquard syndrome is based on physical examination findings. In clinical practice, the pure classic syndrome is rarely seen. Motor examination reveals spastic weakness or paralysis with upper motor neuron signs of increased tone, hyperreflexia, clonus, and a Hoffmann sign on one side of the body. Motor strength of key muscles representing cervical and lumbar spinal root levels should be graded on the standard 0-5 scale. Special care must be taken to test in positions with gravity eliminated and against gravity. The sensory examination is notable for contralateral decreased sensation to light touch and hot or cold. Sensory function should be recorded in representative dermatomes from C2-S4/5 for absent, impaired, or normal sensation to light touch and a pinprick. The findings then can be classified according to the American Spinal Injury Association (ASIA) standard neurological classification of SCI. The neurological level is defined as the most caudal segment with normal function. Complete or incomplete assessment is based on sensory or motor function in S4-S5. The ASIA impairment scale reflects the degree of incomplete injury based on motor and sensory function below the neurological level (see Images 1-2 ). Causes: Brown-Séquard syndrome can be caused by any mechanism resulting in damage to one side of the spinal cord. Multiple causes of Brown-Séquard syndrome have been described in the literature. The most common cause remains traumatic injury, often a penetrating mechanism such as a stab or gunshot wound or a unilateral facet fracture and dislocation due to a motor vehicle accident or fall. Traumatic injury also may be a result of blunt trauma. Numerous nontraumatic causes have also been reported, including tumor (primary or metastatic), multiple sclerosis, disk herniation, herniation of the spinal cord through a dural defect, epidural hematoma, vertebral artery dissection, transverse myelitis, radiation, type II decompression sickness, intravenous drug use, and tuberculosis. Poiseuille's Law...
Recommended Posts