Category Archive Fracture of Bone A-Z

Indications of Total Knee Arthroplasty/Total Knee Arthroplasty (TKA) is one of the most cost-effective and consistently successful surgeries performed in orthopedics. Patient-reported outcomes are shown to improve dramatically with respect to pain relief, functional restoration, and improved quality of life. TKA provides reliable outcomes for patients’ suffering from end-stage, tri-compartmental, degenerative osteoarthritis (OA). While OA affects millions of Americans, the knee is the most commonly affected joint plagued by this progressive condition which is hallmarked by a gradual degeneration and loss of articular cartilage. The most common clinical diagnosis associated with TKA is primary OA, but other potential underlying diagnoses include inflammatory arthritis, fracture (post-traumatic OA and/or deformity), dysplasia, and malignancy.[rx][rx][rx]

Types of Total Knee Arthroplasty

There are 2 main types of surgery:

• Total knee replacement – both sides of your knee joint are replaced
• Partial (half) knee replacement – only 1 side of your joint is replaced in a smaller operation with a shorter hospital stay and recovery period.

Anatomy and Physiology

The knee is a synovial hinge joint with minimal rotational motion. It is comprised of the distal femur, proximal tibia, and the patella. There are 3 separate articulations and compartments: medial femorotibial, lateral femorotibial, and patellofemoral. The stability of the knee joint is provided by the congruity of the joint as well as by the collateral ligaments. The capsule surrounds the entire joint and extends proximally into the suprapatellar pouch. Articular cartilage covers the femoral condyles, tibial plateaus, trochlear groove, and patellar facets. Menisci are interposed in the medial and lateral compartments between the femur and tibia which act to protect the articular cartilage and support the knee.

The mechanical axis of the femur, defined by a line drawn from the center of the femoral head to the center of the knee, is 3 degrees valgus to the vertical axis. The anatomic axis of the femur, defined by a line bisecting the femoral shaft, is 6 degrees valgus to the mechanical axis of the femur and 9 degrees valgus to the vertical axis.[5] The proximal tibia is oriented to 3 degrees of varus. The varus position of the proximal tibia, along with the offset of the hip center of rotation, results in the weight-bearing surface of the tibia is parallel to the ground. The sagittal alignment of the proximal tibia is sloped posteriorly approximately 5 to 7 degrees. The asymmetry of the natural bony anatomy maintains the alignment of the joint and ligamentous tension. The knee is comprised of 2 separate joints: the tibiofemoral and patellofemoral joints.[rx][rx][rx]

Patellofemoral Joint

The patellofemoral joint (PFJ) functions to increase the lever arm of the extensor mechanism. The patella transmits the tensile forces generated by the quadriceps tendon to the patellar tendon. The maximum contact force between the patella and femoral trochlea occurs at 45 degrees of knee flexion, and joint reaction forces reach 7-times body weight in the position of deep squatting.

The quadriceps muscles provide dynamic stability of the PFJ, and passive anatomic restraints include the following:

• Medial patellofemoral ligament: Primary passive restraint against lateral translation at 20 degrees of flexion
• Medial patellomeniscal ligament: Contributes 10% to 15% of the total restraining force
• Lateral retinaculum: Provides 10% of the total restraining force

Tibiofemoral Articulation

The tibiofemoral articulation transmits body weight from the femur to the tibia and generates joint reaction forces of 3 and 4-times body weight during walking and climbing, respectively. Motion occurs in the sagittal plane from 10 degrees of hyperextension to about 140 to 150 degrees of hyperflexion. Extremes of flexion are often limited secondary to direct contact between the posterior thigh and calf. The tibiofemoral contact point and femoral center of rotation move posteriorly with increasing degrees of flexion in order to optimize knee flexion prior to impingement. Normal gait only requires a range of motion (ROM) from 0 to 75 degrees.

Knee stability in the coronal plane is provided by the lateral collateral ligament (LCL), which resists varus stresses, and the medial collateral ligament, which resists valgus stress forces. In addition, the anterior cruciate ligament (ACL) and posterior cruciate ligament (PCL) provide resistance to anteriorly directed and posteriorly directed forces at the knee, respectively.  Resistance to external rotatory forces is provided by the posterolateral corner structures (PLC).

Indications of Total Knee Arthroplasty

Once considered a procedure reserved for the elderly, low-demand patient population, primary TKA is offered more frequently and provides consistent positive outcomes in younger cohorts of patients.  In general, the most common underlying diagnosis associated with performing TKAs across all patient age groups is primary, end-stage, tri-compartmental osteoarthritis.[rx][rx][rx]

TKA is an elective procedure that is, in most cases, reserved for patients experiencing chronic, debilitating symptoms that continue to persist despite the exhaustion of all conservative and nonoperative treatment modalities.

Clinical symptoms of osteoarthritis include

• Knee pain
• Pain with activity and improving with rest
• The pain gradually worsens over time
• Decreased ambulatory capacity

Clinical evaluation includes

• Full knee exam including a range of motion and ligamentous testing
• Knee radiographs include standing anteroposterior, lateral, 45-degree posteroanterior, and skyline view of the patella

Radiographic evidence of osteoarthritis include[rx]

• Joint space narrowing
• Subchondral sclerosis
• Subchondral cysts
• Osteophyte formation

Conservative treatment includes

• Non-steroidal anti-inflammatory medication
• Weight loss
• Activity modification
• Bracing
• Physical therapy
• Viscosupplementation
• Intra-articular steroid injection
• Decreased ambulatory capacity

Clinical evaluation includes

• Full knee exam including range of motion and ligamentous testing
• Knee radiographs include standing anteroposterior, lateral, 45-degree posteroanterior, and skyline view of the patella

Radiographic evidence of osteoarthritis include[rx]

• Joint space narrowing
• Subchondral sclerosis
• Subchondral cysts
• Osteophyte formation

Contraindications of Total Knee Arthroplasty

TKA is contraindicated in the following clinical scenarios

• Local knee infection or sepsis
• Remote (extra-articular), active, ongoing infection or bacteremia
• Severe cases of vascular dysfunction

Absolute

• Active or latent (less than 1 year) knee sepsis
• Presence of active infection elsewhere in body
• Extensor mechanism dysfunction
• Medically unstable patient

Relative

• Neuropathic joint
• Poor overlying skin condition
• Morbid obesity
• Noncompliance due to major psychiatric disorder, alcohol, or drug abuse
• Insufficient bone stock for reconstruction
• Poor patient motivation or unrealistic expectation
• Severe peripheral vascular disease

Equipment of Total Knee Arthroplasty

TKA prosthesis designs have been evolving since the 1950s, beginning with Walldius’ design of the first hinged-knee replacement. In the early 1970s, the total condylar prosthesis (TCP) was the first TKA prosthesis designed to resurface all 3 compartments of the knee. The TCP was a posterior-stabilized design. The 4 main categories of TKA prosthesis designs are listed below in the order of increasing levels of constraint by design.[rx][rx][rx]

Cruciate-Retaining

The cruciate-retaining TKA prosthesis depends on an intact PCL to provide stability inflection. Thus, its use is contraindicated in patients with pre-existing or intra-operatively recognized PCL insufficiency.  Caution is given to any patient presenting with at least moderate instability in any plane of motion, especially PLC instability patients.  PLC instability predisposes the native PCL in a cruciate-retaining TKA to abnormally high stresses and forces, ultimately leading to early failure and TKA instability requiring revision.  Cruciate-retaining TKA is contraindicated in patients suffering from inflammatory arthritic conditions given the increased risk of early PCL attenuation (e.g. Rheumatoid Arthritis).

Proposed advantages of the cruciate-retaining TKA design include:

• Avoidance of tibial post-cam impingement and dislocation
• Retaining more normal anatomy theoretically resembles normal knee kinematics
• Preserved bone stock (less distal femur resected compared to PS TKA prosthesis)
• Native PCL proprioception

Proposed disadvantages of the cruciate-retaining TKA design include:

• A tight PCL can lead to early/accelerated polyethylene wear
• Loose/ruptured PCL results in flexion instability and possible subluxation/dislocation

Multiple meta-analyses have demonstrated satisfactory survivorship and similar outcomes comparing the cruciate-retaining and posterior-stabilized TKA prosthesis designs.

Posterior-Stabilized

The posterior-stabilized TKA design is slightly more constrained and requires the surgeon to sacrifice the PCL. The femoral component contains a cam that is designed to engage the tibial polyethylene post as the knee flexes.

Proposed advantages of the posterior-stabilized TKA design include:

• Facilitates overall balancing of the knee in the setting of an absent PCL
• Theoretically, better knee flexion
• Lower ranges of axial rotation and condylar translation

Proposed disadvantages of the posterior-stabilized TKA design include:

• Cam jump that can result secondary to a loose flexion gap, or in knee hyperextension
• Patellar clunk syndrome
• Tibial post wear and/or fracture

Constrained Nonhinged Design

The constrained nonhinged prosthesis employs a larger tibial post and deeper femoral box, yielding more stability and constraint (within 2 to 3 degrees) in both varus-valgus and internal-external rotatory planes. Indications include collateral ligament attenuation or deficiency, flexion gap laxity, and moderate bone loss in the setting of neuropathic arthropathy. Downsides to this design include not only increased risk of earlier aseptic loosening secondary to the increased inter-component constraint, but also the requirement of more femoral bone resection to accommodate the components.

Constrained Hinged Design

The constrained hinged design is comprised of linked femoral and tibial components. Rotating hinge options allow the tibial bearing to rotate around a yoke that theoretically mitigates the risk of aseptic loosening at the expense of increasing levels of prosthetic constraint. Indications include global ligamentous deficiencies, resections in the setting of tumors, and massive bone loss in the setting of a neuropathic joint.

Other Component Considerations

Modularity and mobile-bearing designs are other noteworthy additional prosthetic design considerations.

Mobile bearing designs allow polyethylene rotation on the tibial baseplate. Although this design concept remains controversial in terms of its generation of reproducibly superior patient-reported outcome measures, advocates cite its utilization and relative indications in younger patient populations secondary to improved wear rates.  However, one notable disadvantage includes the potential for bearing spin-out, which is seen especially in the setting of a loose flexion gap.

All-polyethylene tibial base plates contrast the conventional metal tray with polyethylene inserts (i.e. tibial component modularity) that allow surgeons more flexibility for intra-operative adjustments for fine-tuning TKA stability. A surgeon is able to upsize or downsize the polyethylene after the final tibial implant fixation has been achieved between the metal implant and cement (or bone) interfaces. This allows for a final check and balance step which many TKA surgeons appreciate. In contrast, advocates for the all-polyethylene base plates cite significant cost savings and decreased rates of osteolysis when comparing TKA cohorts, especially in the elderly TKA patient populations.[rx][rx]

Preparation

• Full medical and drug history before surgery
• Appropriate pre-surgical workup, clearance, and optimization
• Pre-operative radiographs of the affected knee
• Pre-operative templating of the affected knee to estimate the component size
• Primary TKA system of choice
• Have various final implant sizes ready and available in the hospital
• Have increasing prosthesis constraint options ready and available in the hospital
• Have revision total knee replacement system of choice ready and available if needed
• +/- antibiotic cement, surgeon preference

Nonoperative Treatment Modalities

According to the 2011 American Academy of Orthopaedic Surgeons (AAOS), Evidence-Based Clinical Guidelines for the treatment of symptomatic hip or knee osteoarthritis, strong or moderately strong recommendations for nonoperative treatment modalities include weight loss, physical activity, physical therapy programs, and NSAIDs and/or tramadol. Other modalities that were not supported by moderate or strong evidence but are often considered reasonable alternative treatment options include but are not limited to acupuncture, chondroitin supplementation, hyaluronic acid injections, corticosteroid injections, lateral wedge insoles, and offloading braces.[rx]

Prosthesis design

• tibial component: high-density polyethylene spacer
• femoral component: metallic component, surfaces contoured similarly to the femoral condyles and trochlea
• patellar component: high-density polyethylene; may be metal-backed

Most designs use polymethylmethacrylate (PMMA) cement for fixation. Cementless designs are available, where fixation is achieved initially by friction, then by ingrowth of bone into the prosthesis.

There are many designs in use, but broadly speaking, TKA is characterized by the degree of constraint, polyethylene spacer fixation, and posterior cruciate ligament (PCL) retention or removal.

Degree of constraint

• unconstrained prostheses – most widely used; the patient’s supporting soft tissues help maintain stability
• semi-constrained implants – more stable, decreased range of motion; closely conforming tibial and femoral components
• constrained implants – hinged mechanism; most stable, but most limited range of motion, meaning more mechanical stress and susceptibility to wear, fatigue, and loosening; usually used in:
  • revision arthroplasty
  • elderly patients with highly unstable ligaments
  • combination with tumor resection

Spacer fixation

• fixed bearing: the tibial spacer is fixed in a metal tibial tray
• mobile bearing: a mobile polyethylene insert glides along the surface of the metallic tibial component

PCL retention vs removal

The PCL, an important knee stabilizer, can be:

• retained; this is usually the case with unconstrained prostheses
• removed
• removed and substituted for by a PCL-substituting mechanism in the prosthesis

The decision whether to retain or remove the PCL depends mostly on the surgeon’s preference and experience.

Radiographic features

Plain radiograph

The most cost-effective and commonest method of follow-up. Baseline radiographs should be obtained immediately post-operation.

Normal appearance on routine views:

• AP
  • mechanical axis corrected to 0 degrees, results in femoral component placed 5-9 degrees valgus to long axis of femur
  • tibial component: aligned perpendicular to long axis of tibia
  • polyethylene (radiolucent) spacer in tibiofemoral joint space: equal width medially and laterally; NB: beam angle, patient positioning or post-op flexion contracture may distort this
• lateral
  • femoral component: perpendicular to long femoral axis, unless surgeon has chosen to flex component by up to 3 degrees
  • tibial component: perpendicular to long tibial axis or posteriorly inclined by up to 5 degrees
  • patella: anterior and articular sides parallel to each other. Oblique patella on true lateral view suspicious for subluxation, patella Alta for patellar tendon rupture, and significant patella baja for quadriceps tendon rupture
• skyline Merchant view
  • for assessing patellofemoral alignment: patellar component should be centered above femoral component trochlea

CT and MRI

True axial imaging allows assessing for the rotational alignment of the femoral component. To this end, two lines are drawn, which should be parallel:

• transepycondylar line, or axis: drawn between the sulcus of medial epicondyle and peak of the lateral epicondyle
• a second line is drawn across the posterior margins of the femoral component
• if the lines diverge medially, the component is externally rotated: can cause an increased medial flexion gap and result in flexion instability
• if they diverge laterally, the component is internally rotated: early or delayed patellofemoral complications may ensue, especially if internal rotation exceeds 5 degrees

Preoperative Evaluation: Clinical Examination

A thorough history and physical examination are required before performing a TKA in any patient. Patients should be asked about any and all previous interventions and treatments. Prior joint replacements, arthroscopic procedures, or other surgeries around the knee should be considered. Old surgical scars can affect the planned surgical approach. In addition, patients with a history of prior injuries or procedures can present with mechanical axis deformities, retained hardware, or knee instability in any plane. A multitude of factors can impact the TKA prosthesis of choice that is most appropriate for the patient.

We recommend each patient pursuing elective TKA surgery first receive a comprehensive medical evaluation with any appropriate medical optimization tests performed before the TKA procedure. A surgeon must consider the relevant risks and potential benefits of performing TKA on a case-by-case basis.

Physical examination includes evaluation of the overall mechanical axis of the limb. It is critical to ensure hip pathology is either ruled out or at least considered before performing any surgery around the knee. The vascular status of the limb should also be assessed by observing the skin for any chronic venous stasis changes, cellulitis, or even wounds/ulcerations that may be present on the extremity. Distally, the pulses should be symmetric and palpable. Consideration should be given for a vascular surgeon consultation in the preoperative setting in any patient presenting with peripheral vascular disease (PVD). The surgeon should also be aware of the possibility of PVD presenting as knee pain out of proportion in the setting of relatively benign radiographs.

The preoperative range of motion should be noted at the knee and adjacent joints (hip, ankle). The soft tissues should be examined for evidence of gross atrophy, overall symmetry, and ligamentous stability in all planes at the knee joint. It is essential to document the presence of any laxity in the varus/valgus plane and the ability to correct the deformity. These parameters help prepare the surgeon for soft tissue releases that may be required to facilitate mechanical axis correction, as well as plan for additional bone resection that may be needed in the setting of significant contractures.

Preoperative Evaluation: Radiographs

Preoperative radiographs, including a weight-bearing anteroposterior (AP) view, are evaluated for overall mechanical alignment, the presence of deformity, and bone loss. The tibiofemoral angle can help estimate the magnitude of coronal deformity. The femoral resection angle is calculated as the difference between the mechanical and anatomic axis of the femur. The lateral view of the knee is essential for appreciating the native posterior slope of the proximal tibia as well as the presence of posterior osteophytes on the femoral condyles.

The patellofemoral radiographic view is not necessary for TKA templating but allows the surgeon to evaluate the magnitude of patellofemoral arthritis and deformity. In cases of advanced patellofemoral deformity, osteophyte removal may be needed prior to attempting to evert the patella during the procedure. In addition, a surgeon can plan for a possible lateral release to improve patellar tracking.

Technique

The goal of TKA is the same regardless of surgeon, implant, or technique. The variability in the procedure lies in the technique.  Some of the variations in the operative technique for TKA are listed below.

• General anesthesia versus regional anesthesia
• Tourniquet versus tourniquet-less surgery
• Standard versus patient-specific instrumentation
• Standard versus patient-specific implants
• Traditional versus robotic-assisted TKA
• Traditional versus navigation-assisted TKA
• Traditional versus sensor-assisted TKA
• Measured resection versus gap balancing
• Cruciate-retaining implant versus cruciate stabilized the implant
• Resurfaced versus non-resurfaced patella
• Cement versus cement-less (press fit) TKA

Surgical Approaches

The most common approaches for the standard primary TKA procedure include the medial parapatellar, midvastus, and subcastes approach.  The medial parapatellar approach is commonly utilized and entails proximal dissection through a medial cuff of the quadriceps tendon to facilitate superior tissue quality closure at the conclusion of the procedure. Distally, a meticulous, continuous medial subperiosteal dissection sleeve is performed while maintaining intimacy with the proximal tibial bone. The extent of dissection is often dictated by the anticipated amount of deformity to be corrected. In general, this medial release is aggressive in cases of severe varus deformity, and most minimal in cases of moderate to advanced valgus knee deformity. The medial meniscus is also resected with this sleeve of soft tissue.[rx][rx][rx]

Alternatives to the standard medial parapatellar arthrotomy include the midvastus and subvastus approaches. The midvastus approach spares the quadriceps tendon. Instead, the vastus medialis obliquus (VMO) muscle belly is dissected along a trajectory directed toward the superomedial aspect of the proximal pole of the patella.

The subvastus approach also spares the quadriceps tendon and lifts the muscle belly of the VMO off the intermuscular septum. The subvastus approach preserves the vascularity of the patella and is cautioned as it can limit exposure in particularly challenging cases or in particularly obese patients.

Procedural Steps

Depending on surgeon preference, the specific order of bone resections and soft tissue releases will vary. However, a general overview of a preferred method is the goal of this technical summary of the TKA procedure.

Once the arthrotomy is complete, the patella is everted, and the knee is flexed with additional soft tissue releases required prior to achieving knee dislocation.  If the surgeon elects to proceed with the femur first, an intramedullary (IM) drill is utilized in order to gain access to the femoral canal for the utilization of a distal femoral IM jig. The angle set on the guide is based on the patient-specific preoperative evaluation (AP Xray), generally yielding 5 or 7 degrees of valgus. Although system-specific, most surgeons prefer resecting 9 to 10 mm of the distal femur.

Next, the proximal tibia is cut utilizing an IM or extramedullary (EM) guide with the goal of cutting the bone perpendicular (or within 2 to 3 degrees of varus for surgeons aiming for an “anatomic” TKA procedure) to the tibial axis. We prefer an IM guide and a perpendicular tibial cut. The rotation is set referencing the medial one-third of the tibial tubercle (proximally) and a point slightly medial to the center of the ankle joint (distally). This alignment is also referenced with the second ray of the foot and the tibial crest.

Once the tibial cut is performed, the extension gap can be assessed. A spacer block is then inserted with the knee in full extension, and the overall balance of the knee is assessed using an alignment rod to facilitate and verify overall varus-valgus and tibial slope parameters achieved.

Next, the flexion gap is attained after utilizing an AP sizing guide that is positioned with respect to the bony landmarks on the femur (usually Whiteside’s line or the native transepicondylar axis [TEA]). Depending on the anterior or posterior referencing style of the operating surgeon, the flexion gap is set and adjusted as needed utilizing the system-specific incremental sizing adjustments available with respect to the cutting guides. Prior to making the bony cuts, the flexion gap should be visualized, and soft tissue balancing appreciated. A spacer block can facilitate this assessment. The surgeon should ensure a rectangular flexion gap will be the ultimate result after the bone resections. After satisfactory check and balancing steps are verified, the anterior, posterior, anterior chamfer and posterior chamfer cuts are made. Care is taken to protect the collateral soft tissue structures (LCL, MCL) with retractors.

Next, the intercondylar notch cut is made perpendicular to the TEA. The attention is again turned back to the proximal tibia to finish preparation, sizing, and rotational alignment. One must be cautious to avoid internal rotation and/or component overhang which can lead to inferior TKA results. The femoral and tibial trial implants are impacted, and a provisional spacer trial is inserted. The knee is reduced and assessed for stability from 0 degrees of extension through mid-flexion stability.

If planning to resurface the patella, the resection is recommended after first appreciating the native anatomy and size of the entire patellofemoral joint. Inferior TKA outcomes can result from either over-resection, which can compromise implant-bone stock and lead to patella fracture, or under-resection, which can lead to chronic postoperative pain secondary to an overstuffed PFJ.

Finally, the stability parameters are again verified, and patellar tracking is appreciated and must pass intraoperative tracking tests. Most surgeons either use a natural range of motion tracking test to ensure the TKA passes the “no thumb” test, or a towel clip technique can be used.

Patellar maltracking, most commonly occurring laterally, can most often be corrected with a standard lateral release. In more severe cases or in scenarios consistent with component malalignment, consideration should be given to the correction of component position(s).

Wound Closure

The most recent literature remains controversial with respect to the ideal position of the knee and suture material utilized during the TKA closure. Attention to detail is required and a methodical closure is unanimously advocated. A preferred method includes closure with uni- or bi-directional barbed suture for the arthrotomy, deep fascial, and deep dermal/subcutaneous layers. Staples or monocryl can be used for the skin. A sterile dressing is then applied and left in place without being changed for the first 7 days. In addition, a minimal website/ace soft wrap dressing is applied to the knee for, at most, 24 hours to facilitate the appropriate balance between wound healing and postoperative movement of the knee.

Other Considerations

Topical tranexamic acid (TXA) is the preferred application while waiting for the cement to fully harden and prior to dropping the tourniquet. In addition, other controversial technical modalities in TKA include the use of a tourniquet, cementing the patella, femoral, and/or tibial components, as well as incorporating a betadine soak to the wound as part of the copious saline irrigation that is applied prior to closure of the arthrotomy and surgical wound. Preferred techniques include the use of a tourniquet, cementing all components, and saline-only copious pulsatile irrigation prior to arthrotomy closure.

Post-operative Rehabilitation

The length of postoperative hospitalization is 5 days on average depending on the health status of the patient and the amount of support available outside the hospital setting.^[rx] Protected weight bearing on crutches or a walker is required until specified by the surgeon^[rx] because of weakness in the quadriceps muscle^[rx] In the immediate post-operative period, up to 39% of knee replacement patients experience inadequate pain control.^[rx]

To increase the likelihood of a good outcome after surgery, multiple weeks of physical therapy is necessary. In these weeks, the therapist will help the patient return to normal activities, as well as prevent blood clots, improve circulation, increase range of motion, and eventually strengthen the surrounding muscles through specific exercises. Whether techniques such as neuromuscular electrical stimulation are effective at promoting gains in knee muscle strength after surgery are unclear.^[rx] Often a range of motion (to the limits of the prosthesis) is recovered over the first two weeks (the earlier the better). Over time, patients are able to increase the amount of weight-bearing on the operated leg, and eventually are able to tolerate full weight-bearing with the guidance of the physical therapist.^[rx] After about ten months, the patient should be able to return to normal daily activities, although the operated leg may be significantly weaker than the non-operated leg.^[rx]

For post-operative knee replacement patients, immobility is a factor precipitated by pain and other complications. Mobility is known as an important aspect of human biology that has many beneficial effects on the body system.^[rx] It is well documented in the literature that physical immobility affects every body system and contributes to functional complications of prolonged illness.^[rx] In most medical-surgical hospital units that perform knee replacements, ambulation is a key aspect of nursing care that is promoted to patients. Early ambulation can decrease the risk of complications associated with immobilization such as pressure ulcers, deep vein thrombosis (DVT), impaired pulmonary function, and loss of functional mobility.^[rx] Nurses’ promotion and execution of early ambulation on patients has found that it greatly reduces the complications listed above, as well as decreases length of stay and costs associated with further hospitalization.^[rx] Nurses may also work with teams such as physical therapy and occupational therapy to accomplish ambulation goals and reduce complications.^[rx]

Continuous passive motion (CPM) is a postoperative therapy approach that uses a machine to move the knee continuously through a specific range of motion, with the goal of preventing joint stiffness and improving recovery.^[rx][rx] There is no evidence that CPM therapy leads to a clinically significant improvement in range of motion, pain, knee function, or quality of life.^[rx] CPM is inexpensive, convenient, and assists patients in therapeutic compliance. However, CPM should be used in conjunction with traditional physical therapy.^[rx] In unusual cases where the person has a problem that prevents standard mobilization treatment, then CPM may be useful.^[rx]

Cryotherapy, also known as ‘cold therapy’ is sometimes recommended after surgery for pain relief and to limit swelling of the knee. Cryotherapy involves the application of ice bags or cooled water to the skin of the knee joint. However, the evidence that cryotherapy reduces pain and swelling is very weak and the benefits after total knee replacement surgery have been shown to be very small.^[rx]

Some physicians and patients may consider having ultrasonography for deep venous thrombosis after knee replacement.^[rx] However, this kind of screening should be done only when indicated because to perform it routinely would be unnecessary health care.^[rx] If a medical condition exists that could cause deep vein thrombosis, a physician can choose to treat patients with cryotherapy and intermittent pneumatic compression as a preventive measure.

Neither gabapentin nor pregabalin has been found to be useful for pain following a knee replacement.^[rx] A Cochrane review concluded that early multidisciplinary rehabilitation programs may produce better results at the rate of activity and participation.^[rx]

Complications

TKA complications result in inferior outcomes and patient-reported satisfaction scores. Although TKA remains a reliable and reproducibly successful surgery in patients suffering from debilitating advanced degenerative arthritic knees, reports still cite that up to 1 in 5 patients who have undergone primary TKA remain dissatisfied with the outcome.[rx][rx][rx]

Periprosthetic Fracture

TKA periprosthetic fractures (PPFs) are further characterized by location and residual stability of the implants. Distal femur PPFs occur at a 1% to 2% rate, and risk factors include compromised patient bone quality, increased constrained TKA components, and while controversial, anterior femoral notching is a potential risk factor for postoperative fracture.

Tibial PPFs occur at a 0.5% to 1% rate, and risk factors include a prior tibial tubercle osteotomy, component malposition and/or loosening, as well as utilization of long-stemmed components. Patellar PPFs occur less frequently in unresurfaced TKA cases, and incidence rates range from 0.2% up rates as high as 15% or 20%. Risk factors for fracture include osteonecrosis, technical errors in asymmetric or over-resection, and implant-related associations including the following:

• Central, single peg implants
• Uncemented fixation
• Metal-backed components

Aseptic Loosening

TKA aseptic loosening occurs secondary to a macrophage-induced inflammatory response resulting in eventual bone loss and TKA component loosening. Patients often present with pain that is increased during weight-bearing activity and/or recurrent effusions. Patients may have minimal pain at rest or with range of motion. Serial imaging and infectious labs are required to appropriately work up these conditions which eventually are treated with revision surgery if symptoms persist and the patient is considered a reasonable surgical candidate. The steps in aseptic loosening include: particulate debris formation, macrophage-induced osteolysis, micromotion of the components, and dissemination of particulate debris.

Wound Complications

The TKA postoperative wound complication spectrum ranges from superficial surgical infections (SSIs) such as cellulitis, superficial dehiscence and/or delayed wound healing to deep infections resulting in full-thickness necrosis resulting in returns to the operating room for irrigation, debridement (incision and drainage), and rotational flap coverage.

Periprosthetic Joint Infection

The incidence of prosthetic total knee infection (TKA PJI) following primary TKA is approximately 1% to 2% as reported in the literature.  Risk factors include patient-specific lifestyle factors (morbid obesity, smoking, intravenous [IV] drug use and abuse, alcohol abuse, and poor oral hygiene) and patients with a past medical history consisting of uncontrolled diabetes, chronic renal and/or liver disease, malnutrition, and HIV (CD4 counts less than 400). PJI is the most common reason for revision surgery.

The most common offending bacterial organisms in the acute setting include Staphylococcus aureus, Staphylococcus epidermidis, and in chronic TKA PJI cases, coagulase-negative staphylococcus bacteria.  Treatment in the acute setting (less than 3 weeks after index surgery) can be limited to incision and drainage, polyethylene exchange, and retention of components. In addition, IV antibiotics are utilized for up to 4 to 6 weeks duration. Outcomes vary and are often influenced by multiple intraoperative, patient-related factors, and offending bacterial organism, but studies site a 55% successful outcome rate.

More aggressive treatments, especially in the setting of presentation beyond the acute (3 to 4-week time point) include a 1 or 2-stage revision TKA procedure with interval antibiotic spacer placement. The surgeon must ensure and document evidence of infection eradication.

Other Complications and Considerations

Other potential complications after TKA are beyond the scope of this review but include:

• TKA instability – can occur in the coronal or sagittal plane(s).  Also, consideration is given for patellar maltracking or other PFJ issues (for example, overstuffing the joint) in the postoperative setting when patients complain of persistent anterior knee pain
• Extensor mechanism disruption or rupture
• Patellar clunk syndrome – Often occurs 12 months after TKA and is associated with popping, catching during knee extension. It is caused by nodule formation on the posterior quad tendon near its insertion on the patella. Patellar clunk syndrome is associated with posterior stabilized knee design. The cause of scar tissue formation is unknown but the pain results from tissue entrapment in the intercondylar notch. Treatment is surgical, either arthroscopic or open debridement/synovectomy. Conservative measures are often unsuccessful. physical therapy may help with quad strengthening after surgery but is not curative. Recurrence after surgical treatment is rare. More aggressive intervention such as revision TKA is often not warranted in the absence of component malposition.
• Peroneal nerve palsy – One of the most common complications after TKA to correct the valgus deformity. During soft tissue balancing of a valgus knee, the iliotibial band preferentially affects the extension space more than flexion space and inserts on Gerdy’s tubercle. The popliteus is preferentially affected flexion space more than extension space.
• Stiffness
• Vascular injury and bleeding
• Metal hypersensitivity
• Heterotopic ossification[rx][rx]
• Infection, superficial and deep
• Blood clot
• Pulmonary embolism
• Fracture
• Dislocation
• Instability
• Osteolysis resulting in component loosening
• Pain
• Stiffness
• Vascular injury
• Nerve injury

Commonly Required and Suggested Home Preparations

Deep bending and squatting can lead to knee injuries during the recovery period. A patient can minimize these risks by making advanced arrangements and preparing his or her home. For example:

• Arrange for a spouse, friend or other caregiver to provide meals and help around the house.
• Arrange for transportation, as most patients cannot drive for the first 4 to 6 weeks after surgery.
• Stock up on pre-made meals and toiletry items to avoid having to run errands post-surgery.
• If possible, arrange to spend sleeping and waking hours on the same floor in order to avoid stairs.
• If possible, adjust the bed height (not too high or too low) to help ease the transition in and out of bed.
• Take away or move anything that might be tripped over, such as area rugs or electrical cords.
• Make sure all stairs have sturdy railings.
• Install small rails or grab bars near toilets and in showers.
• Install a modified toilet seat; a higher seat will put less stress on the knees and make it easier to sit down and get up.
• Put a small stool in shower to avoid standing on a slippery surface.
• Have a comfortable, supportive chair with an ottoman to keep leg elevated for intervals.
• Have cold packs on hand to help alleviate swelling.
• Consider practicing using walkers, canes and other assistive devices ahead of time to ensure proficiency using them.

References

Intracranial Hemorrhage encompasses four broad types of hemorrhage: epidural hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, and intraparenchymal hemorrhage.[rx][rx][rx] Each type of hemorrhage is different concerning etiology, findings, prognosis, and outcome. This article provides a broad overview of the types of intracranial hemorrhage.

Types of Intracranial Hemorrhage

intracranial hemorrhage

Intra-axial hemorrhage

• signs and formulas
  • • ABC/2 (volume estimation)
    • CTA spot sign
    • swirl sign

• By region or type

• • • basal ganglia hemorrhage
    • cerebellar hemorrhage
      • remote cerebellar hemorrhage
    • cerebral contusions
    • cerebral microhemorrhage
    • ​hemorrhagic venous infarct
    • hemorrhagic transformation of an ischemic infarct
      • cerebral intraparenchymal hyperattenuations post thrombectomy
    • hypertensive intracranial hemorrhage
    • intraventricular hemorrhage (IVH)
    • jet hematoma
    • lobar hemorrhage
      • cerebral amyloid angiopathy
    • pontine hemorrhage
      • Duret hemorrhage
• Extra-axial hemorrhage
  • extradural versus subdural hemorrhage
  • extradural hemorrhage (EDH)
    • venous extradural hemorrhage
  • intralaminar dural hemorrhage
  • subdural hemorrhage (SDH)
    • calcified chronic subdural hemorrhage
  • subarachnoid hemorrhage (SAH)
    • types
      • ruptured berry aneurysm
        • berry aneurysm
        • fusiform aneurysm
        • mycotic aneurysm
      • convexal subarachnoid hemorrhage
      • traumatic subarachnoid hemorrhage (TSAH)
      • perimesencephalic subarachnoid hemorrhage (PMSAH)
    • vasospasm following SAH
    • grading systems
      • Hunt and Hess grading system
      • Fisher scale
      • modified Fisher scale
      • SDASH score
      • WFNS grading system
  • subpial hemorrhage

Causes of Intracranial Hemorrhage

Epidural Hematoma

An epidural hematoma can either be arterial or venous in origin. The classical arterial epidural hematoma occurs after blunt trauma to the head, typically the temporal region. They may also occur after a penetrating head injury. There is typically a skull fracture with damage to the middle meningeal artery causing arterial bleeding into the potential epidural space. Although the middle meningeal artery is the classically described artery, any meningeal artery can lead to arterial epidural hematoma.[rx]

A venous epidural hematoma occurs when there is a skull fracture, and the venous bleeding from the skull fracture fills the epidural space. Venous epidural hematomas are common in pediatric patients.

Subdural Hematoma 

Subdural hemorrhage occurs when blood enters the subdural space which is anatomically the arachnoid space. Commonly subdural hemorrhage occurs after a vessel traversing between the brain and skull is stretched, broken, or torn and begins to bleed into the subdural space. These most commonly occur after a blunt head injury but may also occur after penetrating head injuries or spontaneously.[rx][rx]

Subarachnoid Hemorrhage

A subarachnoid hemorrhage is bleeding into the subarachnoid.  Subarachnoid hemorrhage is divided into traumatic versus non-traumatic subarachnoid hemorrhage. A second categorization scheme divides subarachnoid hemorrhage into an aneurysmal and non-aneurysmal subarachnoid hemorrhage. Aneurysmal subarachnoid hemorrhage occurs after the rupture of a cerebral aneurysm allowing for bleeding into the subarachnoid space. Non-aneurysmal subarachnoid hemorrhage is bleeding into the subarachnoid space without identifiable aneurysms. Non-aneurysmal subarachnoid hemorrhage most commonly occurs after trauma with a blunt head injury with or without penetrating trauma or sudden acceleration changes to the head.[rx]

Intraparenchymal Hemorrhage

Intraparenchymal hemorrhage is bleeding into the brain parenchyma proper. There is a wide variety of reasons due to which hemorrhage can occur including, but not limited to, hypertension, arteriovenous malformation, amyloid angiopathy, aneurysm rupture, tumor, coagulopathy, infection, vasculitis, and trauma.

Pathophysiology

Epidural Hematoma

Epidural hematomas occur when blood dissects into the potential space between the dura and inner table of the skull. Most commonly this occurs after a skull fracture (85% to 95% of cases). There can be damage to an arterial or venous vessel which allows blood to dissect into the potential epidural space resulting in the epidural hematoma. The most common vessel damaged it the middle meningeal artery underlying the temporoparietal region of the skull.

Subdural Hematoma

Subdural hematoma has multiple causes including head trauma, coagulopathy, vascular abnormality rupture, and spontaneous. Most commonly head trauma causes motion of the brain relative to the skull which can stretch and break blood vessels traversing from the brain to the skull. If the blood vessels are damaged, they bleed into the subdural space.

Subarachnoid Hemorrhage

Subarachnoid hemorrhage most commonly occurs after trauma where cortical surface vessels are injured and bleed into the subarachnoid space. Non-traumatic subarachnoid hemorrhage is most commonly due to the rupture of a cerebral aneurysm. When aneurysm ruptures, blood can flow into the subarachnoid space. Other causes of subarachnoid hemorrhage include arteriovenous malformations (AVM), use of blood thinners, trauma, or idiopathic causes.

Intraparenchymal Hemorrhage

Non-traumatic intraparenchymal hemorrhage most often occurs secondary to hypertensive damage to cerebral blood vessels which eventually burst and bleed into the brain. Other causes include rupture of an arteriovenous malformation, rupture of an aneurysm, arteriopathy, tumor, infection, or venous outflow obstruction. Penetrating and non-penetrating trauma may also cause intraparenchymal hemorrhage.

Symptoms of Intracranial Hemorrhage

Symptoms of a brain hemorrhage depend on the area of the brain involved. In general, symptoms of brain bleeds can include:

• Sudden tingling, weakness, numbness, or paralysis of the face, arm or leg, particularly on one side of the body.
• Headache. (Sudden, severe “thunderclap” headache occurs with subarachnoid hemorrhage.)
• Nausea and vomiting.
• Confusion.
• Dizziness.
• Seizures.
• Increasing headache
• A sudden severe headache
• Seizures with no previous history of seizures
• Weakness in an arm or leg
• Decreased alertness; lethargy
• Changes in vision
• Tingling or numbness
• Difficulty speaking or understanding speech
• Difficulty swallowing
• Difficulty writing or reading
• Loss of fine motor skills, such as hand tremors
• Loss of coordination
• Loss of balance
• An abnormal sense of taste
• Drowsiness and progressive loss of consciousness
• Unequal pupil size
• Slurred speech
• Loss of balance or coordination.
• Stiff neck and sensitivity to light.
• Abnormal or slurred speech.
• Difficulty reading, writing or understanding speech.
• Change in level of consciousness or alertness, lack of energy, sleepiness or coma.
• Trouble breathing and abnormal heart rate (if the bleed is located in the brainstem).

Diagnosis of Intracranial Hemorrhage

Epidural Hematoma

Patients with epidural hematoma report a history of a focal head injury such as blunt trauma from a hammer or baseball bat, fall, or motor vehicle collision. The classic presentation of an epidural hematoma is a loss of consciousness after the injury, followed by a lucid interval then neurologic deterioration. This classic presentation only occurs in less than 20% of patients. Other symptoms that are common include severe headache, nausea, vomiting, lethargy, and seizure.

Subdural Hematoma

A history of either major or minor head injury can often be found in cases of subdural hematoma. In older patients, a subdural hematoma can occur after trivial head injuries including bumping of the head on a cabinet or running into a door or wall. An acute subdural can present with recent trauma, headache, nausea, vomiting, altered mental status, seizure, and/or lethargy. A chronic subdural hematoma can present with a headache, nausea, vomiting, confusion, decreased consciousness, lethargy, motor deficits, aphasia, seizure, or personality changes. A physical exam may demonstrate a focal motor deficit, neurologic deficits, lethargy, or altered consciousness.

Subarachnoid Hemorrhage

A thunderclap headache (sudden severe headache or worst headache of life) is the classic presentation of subarachnoid hemorrhage. Other symptoms include dizziness, nausea, vomiting, diplopia, seizures, loss of consciousness, or nuchal rigidity. Physical exam findings may include focal neurologic deficits, cranial nerve palsies, nuchal rigidity, or decreased or altered consciousness.

Intraparenchymal Hemorrhage

Non-traumatic intraparenchymal hemorrhages typically present with a history of sudden onset of stroke symptoms including a headache, nausea, vomiting, focal neurologic deficits, lethargy, weakness, slurred speech, syncope, vertigo, or changes in sensation.

Epidural Hematoma

Initial evaluation includes airway, breathing, and circulation as patients can rapidly deteriorate and require intubation. A detailed neurologic examination helps identify neurologic deficits. With increasing intracranial pressure there may be a Cushing response (hypertension, bradycardia, and bradypnea). Emergent CT head without contrast is the imaging choice of the test due to its high sensitivity and specificity for identifying significant epidural hematomas. Historically cerebral angiography could identify the shift in cerebral blood vessels, but cerebral angiography has been supplanted by CT imaging.[rx][rx][rx]

Laboratory studies should also be considered including a complete blood count to check for thrombocytopenia, coagulation studies (PTT, PT/INR) to check for coagulopathy and basic metabolic panel to check for electrolyte abnormalities.

Subdural Hematoma

After ensuring the medical stability of the patient, a detailed neurologic exam can help identify any specific neurologic deficits. Most commonly a computed tomography (CT) scan of the head without contrast is the first imaging test of choice. An acute subdural hematoma is typically hyperdense with chronic subdural being hypodense. A subacute subdural may be isodense to the brain and more difficult to identify.

Laboratory studies should also be considered including a complete blood count to check for thrombocytopenia, coagulation studies (PTT, PT/INR) to check for coagulopathy and basic metabolic panel to check for electrolyte abnormalities.

Subarachnoid Hemorrhage

Initial evaluation includes assessing and stabilizing the airway, breathing, and circulation (ABCs). Patients with subarachnoid hemorrhage can rapidly deteriorate and may need emergent intubation. A thorough neurologic examination can help identify any neurologic deficits.

The initial imaging for patients with subarachnoid hemorrhage is computed tomography (CT) head without contrast. If the patient is given contrast, this can obscure the subarachnoid hemorrhage. Acute subarachnoid hemorrhage is typically hyperdense on CT imaging. If the CT head is negative and there is still strong suspicion for subarachnoid hemorrhage a lumbar puncture should be considered. The results of the lumbar puncture may show xanthochromia. A lumbar puncture performed before 6 hours of the subarachnoid hemorrhage may fail to show xanthochromia. Additionally, lumbar puncture results may be confounded if a traumatic tap is encountered.

Identifying the cause of non-traumatic subarachnoid hemorrhage will help guide further treatment. Common workup includes either a CT angiogram (CTA) of the head and neck, magnetic resonance angiography (MRA) of the head and neck, or diagnostic cerebral angiogram of the head and neck done emergently to look for an aneurysm, AVM or another source of subarachnoid hemorrhage.

Laboratory studies should also be considered including a complete blood count to check for thrombocytopenia, coagulation studies (PTT, PT/INR) to check for coagulopathy and basic metabolic panel to check for electrolyte abnormalities.

Intraparenchymal Hemorrhage

Once the medical stability of the patient is ensured, CT head without contrast is the first diagnostic test most commonly performed. The imaging should be able to identify acute intraparenchymal hemorrhage as hyperdense within the parenchyma. Depending on the history, physical and imaging findings and patient an MRI brain with and without contrast should be considered as tumors within the brain may present as intraparenchymal hemorrhage. Other imaging to consider include CTA, MRA or diagnostic cerebral angiogram to look for cerebrovascular causes of the intraparenchymal hemorrhage.  Evaluation should also include a complete neurologic exam to identify any neurologic deficits.

Laboratory studies should also be considered including a complete blood count to check for thrombocytopenia, coagulation studies (PTT, PT/INR) to check for coagulopathy and basic metabolic panel to check for electrolyte abnormalities.

Treatment of Intracranial Hemorrhage

Treatment depends substantially on the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.

• Tracheal intubation is indicated in people with a decreased level of consciousness or another risk of airway obstruction.^[rx]
• IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.^[rx]

Medication

• One review found that antihypertensive therapy to bring down the blood pressure in acute phases appears to improve outcomes.^[rx] Other reviews found an unclear difference between intensive and less intensive blood pressure control.^[rx][rx] The American Heart Association and American Stroke Association guidelines in 2015 recommended decreasing the blood pressure to a SBP of 140 mmHg.^[1] However, the evidence finds tentative usefulness as of 2015.^[rx]
• Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.^[rx] It thus overall does not result in better outcomes in those without hemophilia.^[rx]
• Frozen plasma, vitamin K, protamine, or platelet transfusions may be given in case of a coagulopathy. Platelets however appear to worsen outcomes in those with spontaneous intracerebral bleeding on antiplatelet medication.^[rx]
• Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.^[rx]
• H2 antagonists or proton pump inhibitors are commonly given for to try to prevent stress ulcers, a condition linked with ICH.^[rx]
• Corticosteroids were thought to reduce swelling. However, in large controlled studies, corticosteroids have been found to increase mortality rates and are no longer recommended.

Surgery

Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a structural vascular lesion or lobar hemorrhage in a young patient.^[rx]

• A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.^[rx]
• Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.^[rx]
• A craniectomy may take place, were part of the skull is removed to allow a swelling brain room to expand without being squeezed.

Penetrating brain injury (PBI) is a traumatic brain injury (TBI) which is a significant cause of mortality in young individuals. PBI includes all traumatic brain injuries other than blunt head trauma and constitutes the most severe of traumatic brain injuries.[rx][rx][rx][rx]

Causes of Penetrating Brain Injury

Based on the speed of penetration, it can be classified into two categories:

• High-velocity penetration: Examples include injuries caused by bullets or shell fragments, from direct trauma or shockwave injury to surrounding brain tissue due to a stretch injury.
• Low-velocity penetration: Examples include a knife or other sharp objects, with direct trauma to brain tissue.[5]

Pathophysiology

The consequences of penetrating head injury depend on the following factors:

• Intracranial path and location: High mortality resulting from those that cross the midline, pass through the ventricles, or come to rest in the posterior fossa
• Energy and speed of entry: These factors depend on the properties of the weapon or missile. They result from energy being transferred from an object to the human skull and the underlying brain tissue. There is a high mortality rate associated with high-velocity projectiles. The kinetic energy involved is related to the square of the velocity. Three mechanisms of injuries have been reported.

1. Laceration and crushing
2. Cavitation
3. Shockwaves

• Size and type of the penetrating object: Usually, large missiles or missiles that fragment within the cranial vault cause more fatalities
• Circumstances or events surrounding the injury
• Other associated injuries

Primary injuries occur immediately. Secondary injuries occur following the time of the injury. The final neurologic outcome is influenced by the extent and degree of secondary brain injury. Therefore, the primary goal in the emergency department is to prevent or reduce conditions that can worsen outcomes, such as hypotension, hypoxia, anemia, and hyperpyrexia.

The amount of damage to the brain depends on the kinetic energy imparted to the brain tissue. This, in turn, depends on the following factors:

• Trajectories of both the missile and the bone fragments through the brain
• Changes in intracranial pressure at the time of impact.

Diagnosis of Penetrating Brain Injury

The presentation depends on the mechanism, site of the lesions, and associated injuries.

History should include:

• Date and time of injury
• Duration of loss of consciousness (LOC) if present
• Seizure at the time of impact
• Any co-morbidity (if existing)
• Anticoagulants and antiplatelet agents used

Initial physical examination includes primary and secondary trauma survey with the evaluation of other distracting injuries. A complete physical examination should be performed including a neurological examination. This should include documentation of the Glasgow coma scale (GCS). The involvement of cranial nerves should be assessed, and motor/sensory examination should be performed. It is important to realize that neurologic injury may be manifest distant to the site of impact. If unable to fully and formally assess cranial nerves secondary to lack of patient cooperation, it is important to, at least, document any findings relevant to the patient’s neurology.

Evaluation

In the pre-hospital setting, or in non-trauma facilities, stabilize, but, do not remove penetrating objects such as knives. Patients should be transported quickly to a location capable of providing definitive care. Early recognition of high-risk mechanisms, early imaging, and early evaluation at a level 1 trauma center may improve outcomes.[8][9]

In the emergency department, resuscitation and stabilization should be provided. Manage ABCDE’s using Advanced Trauma Life Support (ATLS) guidelines. Perform a primary survey to identify any life-threatening injury. Stabilize, focusing on the airway, breathing, and circulation, including external hemorrhage, while establishing and maintaining cervical spine immobilization. Early activation of a trauma team may help to provide prompt recognition of polytrauma. The target is to maintain a systolic blood pressure of at least 90 mm Hg.

Following initial resuscitation and stabilization, an inspection of the superficial wound should be performed. Identify the entrance wound (and exit wounds, if present). Beware that blood-matted hair may cover these wounds. When a patient presents with a gunshot wound to the head, the other parts of the body including neck, chest, and abdomen should be inspected carefully for other gunshot wounds. Beware that injuries to the heart or great vessels in the chest or abdomen may be even more life-threatening.

A subgaleal hematoma can become extensive because blood easily dissects through the loose areolar tissue; such a hematoma can be a cause of hemodynamic compromise. Apply a sterile dressing to both the entrance and exit wounds. Assess whether there is any oozing of cerebrospinal fluid (CSF), blood, or brain parenchyma from the wound. Evaluate for hemotympanum, which may indicate a basilar skull fracture. Examine all orifices for retention of foreign bodies, the missile, teeth, and bone fragments.

Perform neurological examination, including GCS and document well. Evaluating for signs suggesting raised intracranial pressure is critical. The initial signs and symptoms may be nonspecific and include a headache, nausea, vomiting, and papilledema.

Perform a careful examination of the neck, chest, abdomen, pelvis, and extremities. Assume multiple injuries in cases of penetrating trauma. Obtain a detailed history including the “AMPLE” history with an emphasis on events surrounding the injury. Also, determine the weapon type and/or caliber of the weapon.

CT Scan

If the patient is hemodynamically stable, obtain a Computed Tomography (CT) scan of the head to evaluate for the presence of a mass lesion (hematoma) or cerebral edema. It can be obtained when the patient is stabilized and ready to be transported to the radiology department. A CT scan can adequately identify the extent of the intracranial injury and can also determine the relationship between the penetrating object and the intracranial structures. However, a radiolucent object, such as a wooden object, maybe missed by the CT scan. In patients with penetrating head trauma, a large mass or hematoma may be evident. If ICP is increased, aqueductal stenosis is present, and the third but not fourth ventricle is enlarged.

Certain factors are important in critical decision making and have prognostic implications. These may include the following:

• Sites of entry and exit wounds
• Presence of intracranial fragments
• Missile track and its relationship to both blood vessels and air-containing skull-base structures
• Presence of intracranial air
• Trans-ventricular injury
• Basal ganglia and brain stem injury
• Whether the missile track cross the midline
• Presence of multi-lobar injury
• Presence of basal cistern effacement
• Brain parenchymal herniation
• Presence of any associated mass effects

Plain Radiograph

Maybe useful as it provides information about the following:

• Shape of the penetrating object
• Skull fractures (if present)
• An intracranial foreign object (if present)

Computed Tomographic Angiography (CTA)

• If a vascular injury is suspected, noninvasive investigative CTA should be obtained after patient stabilization.

Magnetic Resonance Imaging (MRI) Scan

• Additionally, an MRI Scan may be obtained if penetrating objects are suspected to be wooden objects. It should not be performed if intracranial metallic fragments are present. Such a procedure is contraindicated. However, if no bullets or intracranial metallic fragments are present, then an MRI scan of the brain can be performed in a stable patient. This can provide information about the posterior fossa structures and the extent of possible shared injuries.

Treatment of Penetrating Brain Injury

Patients with penetrating head trauma require both medical and surgical management.[rx][rx][rx]

Antibiotics – Intravenous co-amoxiclav 1.2g q8h OR intravenous cefuroxime 1.5g, then 750mg q8h AND intravenous metronidazole 500mg q8h for 7-14 days[rx][rx]

Anticonvulsants – Prophylactic phenytoin, carbamazepine, valproate, or phenobarbital is usually given in the first week after an injury[rx] Seizures may happen – The doctor may give you antiseizure medicines. Strong pain relievers, like opioids, may be given through an IV.

Medical Management

A low threshold for obtaining surgical consultation should be considered in cases of penetrating head trauma. Beware that many patients with penetrating head trauma will likely require operative intervention.

Indeed, do not remove any penetrating object from the skull in the emergency department until trauma and neurosurgical evaluation is obtained. Also, the protruding object should be stabilized, and provision should be made to protect it from moving during transportation of the patient, to prevent further injury.

Assess the need for endotracheal intubation.

• Inability to maintain adequate ventilation
• Inability to protect the airway due to depressed level of consciousness
• Neck or pharyngeal injury

Normalize PCO2. Avoid hyperventilation, because it leads to vasoconstriction and a subsequent reduction in the cerebral perfusion pressure (CPP). This may worsen long-term neurological outcome. Beware that hyperventilation is only a temporizing measure for the reduction of elevated intracranial pressure (ICP). Avoid hyperventilation during the first 24 hours after injury when cerebral blood flow (CBF) often is reduced.

Monitor intracranial pressure (ICP) particularly in patients with GCS less than 8. Consider head elevation to 30 degrees. This can improve venous drainage and may decrease ICP. The target is to maintain intracranial pressure (ICP) less than 20 mmHg to 25 mmHg and CPP greater than 70 mmHg. Since cerebral blood flow (CBF) is difficult to measure continuously, the CPP is measured as a surrogate. Treatment typically is indicated for ICP greater than or equal to 20 mmHg to 25 mmHg, with guideline goals of ICP less than 20 mmHg and cerebral perfusion pressure (CPP) 50 mmHg to 70 mmHg.

Surgical Management

A major reason for surgical intervention is the presence of a hematoma. Large hematomas should be evacuated promptly. Early decompression with conservative debridement of the brain may be needed. In most cases, the removal of a deep-seated bullet may not be required. However, there are certain indications when removal should be considered. These are:

• Penetrating injury through pterion, orbit, or posterior fossa
• Presence of intracranial hematoma
• Presence of pseudoaneurysm at the time of initial exploration

A craniotomy is needed for low-velocity missile wounds in which the object is still protruding from the head. Some critical factors can determine the outcome for those who survive the initial injury; they depend on prompt and early surgical intervention as well as the ability to provide high-level neurocritical care.

• http://rxharun.com/symptoms-vitamin-e-deficiency-food-source/
• https://www.ncbi.nlm.nih.gov/books/NBK459254/

A Head Injury is any injury that results in trauma to the skull or brain. The terms traumatic brain injury and head injury are often used interchangeably in the medical literature. Because head injuries cover such a broad scope of injuries, there are many causes including accidents, falls, physical assault, or traffic accidents that can cause head injuries.

Head injuries include injuries to the brain and those to other parts of the head, such as the scalp and skull. Head injuries can be closed or open. A closed (non-missile) head injury is where the dura mater remains intact. The skull can be fractured, but not necessarily. A penetrating head injury occurs when an object pierces the skull and breaches the dura mater. Brain injuries may be diffuse, occurring over a wide area, or focal, located in a small, specific area. A head injury may cause a skull fracture, which may or may not be associated with injury to the brain. Some patients may have linear or depressed skull fractures. If intracranial hemorrhage occurs, a hematoma within the skull can put pressure on the brain. Types of intracranial hemorrhage include subdural, subarachnoid, extradural, and intraparenchymal hematoma. Craniotomy surgeries are used in these cases to lessen the pressure by draining off the blood.

Traumatic brain injury (TBI) is a common presentation in emergency departments, which accounts for more than one million visits annually. It is a common cause of death and disability among children and adults.[rx]

Based on the Glasgow Coma Scale (GCS) score, it is classified as:

• Mild = GCS 13 to 15, also called concussion
• Moderate = GCS 9 to 12
• Severe = GCS 3 to 8

Types of Head Injury

TBI can be classified as primary injury and secondary injury

Primary Injury

Primary injury includes injury upon the initial impact that causes displacement of the brain due to direct impact, rapid acceleration-deceleration, or penetration. These injuries may cause contusions, hematomas, or axonal injuries.

• Contusion (bruise on the brain parenchyma)
• Hematoma (subdural, epidural, intraparenchymal, intraventricular, and subarachnoid)
• Diffuse axonal injury (stress or damage to axons)

Secondary Injury/Secondary Neurotoxic Cascade

Secondary injury consists of the changes that occur after the initial insult. It can be due to

• Systemic hypotension
• Hypoxia
• Increase in ICP

After a primary brain injury, a cascade of cellular and biochemical events occurs which include the release of glutamate into the presynaptic space resulting in activation of N-methyl-D-aspartate, a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, and other receptors. This ionic shift may activate cytoplasmic and nuclear enzymes, resulting in mitochondrial damage, and cell death and necrosis.

Brain Herniation

Herniation occurs due to increased ICP. The following are the types of herniations.

1) Uncal transtentorial

• The uncus is the most medial portion of the hemisphere, and the first structure to shift below the tentorium.
• Compression of parasympathetic fibers running with the third cranial nerve
• Ipsilateral fixed and dilated pupil with contralateral hemiparesis

2) Central transtentorial

• Midline lesions, such as lesions of the frontal or occipital lobes or vertex
• Bilateral pinpoint pupils, bilateral Babinski signs, and increased muscle tone. Fixed midpoint pupils follow along with prolonged hyperventilation and decorticate posturing

3) Cerebellar tonsillar

• Cerebellar tonsils herniate in a downward direction through the foramen magnum
• Compression on the lower brainstem and upper cervical spinal cord
• Pinpoint pupils, flaccid paralysis, and sudden death

4) Upward posterior fossa/cerebellar herniation

• The cerebellum is displaced in an upward direction through the tentorial opening
• Conjugate downward gaze with an absence of vertical eye movements and pinpoint pupils

Pathophysiology

The following concepts are involved in the regulation of blood flow and should be considered.

1) Monroe-Kellie Doctrine

• Related to the understanding of intracranial pressure (ICP) dynamics.
• Any individual component of the intracranial vault may undergo alterations, but the total volume of intracranial contents remains constant since the space within the skull is fixed. In other words, the brain has a compensatory mechanism to maintain an equilibrium thereby maintaining normal intracranial pressure.
• According to this, the displacement of cerebrospinal fluid (CSF) or blood occurs to maintain normal ICP. A rise in ICP will occur when the compensatory mechanisms are exhausted.

2) Regulation of Cerebral Blood Flow (CBF) (Autoregulation)

• Under normal circumstances, the brain maintains CBF via auto-regulation which maintains equilibrium between oxygen delivery and metabolism.
• Autoregulation adjusts Cerebral perfusion pressure (CPP) from 50 to 150 mm Hg. Beyond this range, autoregulation is lost, and blood flow is only dependent on blood pressure.
• Severe brain injury may disrupt the autoregulation of CBF.

3) Cerebral Perfusion Pressure (CPP)

• The difference between the mean arterial pressure (MAP) and the ICP (CPP = MAP – ICP)
• Target CPP is 55 mm Hg  to 60 mm Hg
• An increase in ICP can decrease the CPP
• A decrease in ICP may improve CPP
• Remember, lowering MAP in a hypotensive patient may lower CPP.
• A minimum CPP should be maintained to avoid cerebral insult. It is age-dependent and is as follows: Infants – 50 mm Hg, Children – 60 mm Hg, and Adults – 70 mm Hg.
• CBF is quite sensitive to oxygen and carbon dioxide.
• Hypoxia causes vasodilation and therefore increases CBF and may worsen ICP.
• Hypercarbia also results in vasodilation and can alter ICP via effects on cerebrospinal fluid (CSF) pH and increases CBF.

4) Mean arterial pressure (MAP)

• Maintain = 80 mm Hg
• 60 mm Hg = cerebral vessels maximally dilated
• < 60 mm Hg = cerebral ischemia
• > 150mmHg =  increased ICP

5) Intracranial pressure (ICP)

• An increase in ICP can decrease CPP.
• ICP is dependent on the volume of the following compartments:
• Brain parenchyma (< 1300 mL)
• Cerebrospinal fluid (100 – 150 mL)
• Intravascular blood (100 – 150 mL)
• Cushing reflex (hypertension, bradycardia, and respiratory irregularity) due to an increase in ICP
• Normal ICP is age-dependent (adult younger than ten years old, child 3-7 years old, infant 1.5-6 years old)
• > 20 mm Hg= increased morbidity and mortality and should be treated. It is perhaps more important to maintain an adequate CPP.

Causes of Head Injury

The leading causes of head trauma are

• (1) motor vehicle-related injuries,
• (2) falls, and
• (3) assaults.[rx][rx]

Based on the mechanism, head trauma is classified as

• (1) blunt (the most common mechanism),
• (2) penetrating (most fatal injuries),
• (3) blast.

Specific problems after a head injury can include

Diagnosis of Head Injury

Evaluation

CT scan is required in patients with head trauma

• Moderate (GCS score 9 to 12)
• Severe (GCS score < 8)

For patients who are at low risk for intracranial injuries, there are two externally validated rules for when to obtain a head CT scan after TBI.[rx][rx] It is important to understand that no individual history and physical examination findings can eliminate the possibility of intracranial injury in head trauma patients. Skull x-rays are only used to assess for foreign bodies, gunshots or stab wounds

New Orleans Criteria

• Headache
• Vomiting (any)
• Age > 60 years
• Drug or alcohol intoxication
• Seizure
• Trauma visible above clavicles
• Short-term memory deficits

Canadian CT Head Rule

• Dangerous mechanism of injury
• Vomiting = two times
• Age > 65 years
• GCS score < 15, 2-hours post-injury
• Any sign of basal skull fracture
• Possible open or depressed skull fracture
• Amnesia for events 30 minutes before injury

Level A Recommendation

With the loss of consciousness or posttraumatic amnesia only if one or more of the following symptoms are present:

• Headache
• Vomiting
• Age > 60 years
• Drug or alcohol intoxication
• Deficits in short-term memory
• Physical findings suggestive of trauma above the clavicle
• Posttraumatic seizure
• GCS score < 15
• Focal neurologic deficit
• Coagulopathy

Level B Recommendation

Without loss of consciousness or posttraumatic amnesia if one of the following specific symptoms presents:

• Focal neurologic deficit
• Vomiting
• Severe headache
• Age > 65 years
• Physical signs of a basilar skull fracture
• GCS score < 15
• Coagulopathy
• Dangerous mechanism of injury
• Ejection from a motor vehicle (such as Pedestrian struck or a fall from a height > three feet or five stairs)

The risk of intracranial injury when clinical decision rule results are negative is less than 1%. For children, Pediatric Emergency Care Applied Research Network (PECARN) decision rules exist to rule out the presence of clinically important traumatic brain injuries. However, this rule applies only to children with GCS > 14.

CT Scan

• If the patient is hemodynamically stable, obtain a Computed Tomography (CT) scan of the head to evaluate for the presence of a mass lesion (hematoma) or cerebral edema. It can be obtained when the patient is stabilized and ready to be transported to the radiology department.
• A CT scan can adequately identify the extent of the intracranial injury and can also determine the relationship between the penetrating object and the intracranial structures. However, a radiolucent object, such as a wooden object, maybe missed by the CT scan.
• In patients with penetrating head trauma, a large mass or hematoma may be evident. If ICP is increased, aqueductal stenosis is present, and the third but not fourth ventricle is enlarged.

Certain factors are important in critical decision making and have prognostic implications. These may include the following:

• Sites of entry and exit wounds
• Presence of intracranial fragments
• Missile track and its relationship to both blood vessels and air-containing skull-base structures
• Presence of intracranial air
• Trans-ventricular injury
• Basal ganglia and brain stem injury
• Whether the missile track cross the midline
• Presence of multi-lobar injury
• Presence of basal cistern effacement
• Brain parenchymal herniation
• Presence of any associated mass effects

Plain Radiograph

Maybe useful as it provides information about the following:

• Shape of the penetrating object
• Skull fractures (if present)
• An intracranial foreign object (if present)

Computed Tomographic Angiography (CTA)

• If a vascular injury is suspected, noninvasive investigative CTA should be obtained after patient stabilization.

Magnetic Resonance Imaging (MRI) Scan

• MRI Scan may be obtained if penetrating objects are suspected to be wooden objects. It should not be performed if intracranial metallic fragments are present. Such a procedure is contraindicated. However, if no bullets or intracranial metallic fragments are present, then an MRI scan of the brain can be performed in a stable patient. This can provide information about the posterior fossa structures and the extent of possible shared injuries.

Treatment of Head Injury

The most important goal is to prevent secondary brain injuries. This can be achieved by the following:

• Maintain airway and ventilation
• Maintain cerebral perfusion pressure
• Prevent secondary injuries (by recognizing and treating hypoxia, hypercapnia, or hypoperfusion)
• Evaluate and manage for increased ICP
• Obtain urgent neurosurgical consultation for intracranial mass lesions
• Identify and treat other life-threatening injuries or conditions (if they exist)

A relatively higher systemic blood pressure is needed:

• Increase in intracranial pressure
• Loss of autoregulation of cerebral circulation

Priorities remain the same:  the ABC also applies to TBI. The purpose is to optimize perfusion and oxygenation.[rx][rx][rx]

Positioning

• Though it is unclear whether elevating the head of the bed is clearly beneficial, elevation to 30 degrees is recommended in the setting of suspected increased ICP.[rx]

Airway and Breathing

Identify any condition which might compromise the airway, such as pneumothorax. For sedation, consider using short-acting agents having minimal effect on blood pressure or ICP:

• Induction agents:  Etomidate or propofol
• Paralytic agents: Succinylcholine or Rocuronium

Consider endotracheal intubation in the following situations:

• Inadequate ventilation or gas exchange such as hypercarbia, hypoxia, or apnea
• Severe injury (GCS score of = 8)
• Inability to protect the airway
• Agitated patient
• Need for patient transport

The cervical spine should be maintained in-line during intubation. Nasotracheal intubation should be avoided in patients with facial trauma or basilar skull fracture.

Targets:   

• Oxygen saturation > 90
• PaO2 > 60
• PCO at 35 – 45

Circulation

Avoid hypotension. Normal blood pressure may not be adequate to maintain adequate flow and CPP if ICP is elevated.

Target

• Systolic blood pressure > 90 mm Hg
• MAP > 80 mm Hg

Isolated head trauma usually does not cause hypotension. Look for another cause if the patient is in shock.

Increased ICP

Increased ICP can occur in head trauma patients resulting in the mass occupying lesion. Utilize a team approach to manage impending herniation.

Signs and symptoms:

• Change in mental status
• Irregular pupils
• Focal neurologic finding
• Posturing: decerebrate or decorticate
• Papilledema (may not be apparent with a rapid elevation of ICP)

CT scan findings:

• Attenuation of sulci and gyri
• Poor gray/white matter demarcation

General Measures

• Head Position – Raise the head of the bed and maintain the head in midline position at 30 degrees: potential to improve cerebral blood flow by improving cerebral venous drainage.
• Lower cerebral blood volume – (CBV) can lower ICP.
• Temperature Control – Fever should be avoided as it increases cerebral metabolic demand and affects ICP.
• Seizure prophylaxis – Seizures should be avoided as they can also worsen CNS injury by increasing the metabolic requirement and may potentially increase ICP. Consider administering fosphenytoin at a loading dose of 20mg/kg. Only use an anticonvulsant when it is necessary, as it may inhibit brain recovery.
• Fluid management – The goal is to achieve euvolemia. This will help to maintain adequate cerebral perfusion. Hypovolemia in head trauma patients is harmful. Isotonic fluid such as normal saline or Ringer Lactate should be used. Also, avoid hypotonic fluid.
• Sedation – Consider sedation as agitation and muscular activity may increase ICP.
• Fentanyl – Safe in intubated patients
• Propofol – A short-acting agent with good sedative properties, the potential to lower ICP, possible risk of hypotension and fatal acidosis
• Versed – sedative, anxiolytic, possible hypotension
• Ketamine – Avoid as it may increase ICP.
• Muscle relaxants – Vecuronium or Rocuronium are the best options for intubation; Succinylcholine should not be used as ICP may rise with fasciculations.

 ICP monitoring

• Severe head injury
• Moderate head injury with increased risk factors such as abnormal CT scan finding
• Patients who cannot be evaluated with serial neurological examination
• ICP monitoring is often done in patients with severe trauma with a GCS of less than 9. The reference range for normal CIP is 2-15 mmHg. In addition, the waveform of the tracing is important.

Hyperventilation

• Normocarbia is desired in most head trauma patients. The goal is to maintain PaCO between 35-45 mmHg. Judicious hyperventilation helps to reduce PaCO2 and causes cerebral vasoconstriction. Beware that, if extreme, it may reduce CPP to the point that exacerbation of secondary brain injury may occur. Avoid hypercarbia: PaCO > 45 may cause vasodilatation and increases ICP.

Mannitol

• A potent osmotic diuretic with net intravascular volume loss
• Reduces ICP and improves cerebral blood flow, CPP, and brain metabolism
• Expands plasma volume and can improve oxygen-carrying capacity
• The onset of action is within 30 minutes
• Duration of action is from two to eight hours
• Dose is 0.25-1 g/kg (maximum: 4 g/kg/day)

Avoid serum sodium > 145 m Eq/L

• Serum sodium > 145 m Eq/L
• Serum osmolality > 315 mOsm

Relative contraindication

• hypotension does not lower ICP in hypovolemic patients.

Hypertonic saline – May be used in hypotensive patients or patients who are not adequately resuscitated.

• The dose is 250 mL over 30 minutes.
• Serum osmolality and serum sodium should be monitored.
• Hypothermia may be used to lower cerebral metabolism but it is important to be aware that hypothermia also makes the patient susceptible to infections and hypotension.

Initial treatment should focus on the ABCs with the goal of maintaining cerebral perfusion and oxygenation.

Glucose

• In patients with moderate to severe TBI, avoiding hyperglycemia is recommended. An insulin drip may be needed to maintain a goal of 100-180 mg/dL.[rx]

Temperature

• As fever can increase the metabolic demand of the brain, and may increase ICP, treat fever aggressively with a goal of normothermia. At this time, therapeutic hypothermia for TBI is not recommended.

Seizures

• Since seizures are a common sequela of CHI and may worsen secondary injury, treat acute seizures with benzodiazepines. Seizure prophylaxis is more controversial but is recommended in patients with GCS <10, penetrating injury, depressed skull fracture, cortical contusion, intracranial hematoma, or seizure within the first 24 hours of head injury. Levetiracetam has shown to be as effective as phenytoin, but there is currently no recommendation as to the superiority of either agent to prevent seizures.[rx][rx]

Elevated ICP and Herniation

• Early consultation with neurosurgery in the setting of moderate to severe TBI is recommended. Neurosurgery will help to direct surgical interventions and ICP assessment and monitoring with devices such as an intracranial bolt or external ventricular drain (EVD).

A sustained ICP >20 mmHg is associated with increased morbidity and mortality,  The Brain Trauma Foundation lists the following indications for invasive intracranial pressure monitoring:

• 1) Moderate to severe TBI in patients who cannot be accurately serially assessed by physical examination (for example intubated patients);
• 2) Severe head injury with abnormal CT scan;
• 3) Severe head injury with a normal CT if 2 of the following: age >40, systolic BP <90 mmHg, or abnormal motor posturing.

References