An Overview of Consent and Restraint
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Deliberate or implied affirmation; compliance with a course of proposed action. Consent is essential in a number of circumstances. For example, contracts and marriages are invalid unless both parties give their consent. Consent must be given freely, without duress or deception, and with sufficient legal competence to give it (see also INFORMED CONSENT). In criminal law, issues of consent arise mainly in connection with offences involving violence and *dishonesty. For public-policy reasons, a victim’s consent to conduct which foreseeably causes him bodily harm is no defence to a charge involving an *assault, *wounding, or *homicide; in other cases the defendant should be acquitted if the magistrates or jury have a reasonable doubt not only as to whether the victim had consented but also as to whether he thought the victim had consented.
Restraint, assault and an intentional or reckless act that causes someone to be put in fear of immediate physical harm. Actual physical contact is not necessary to constitute an assault (for example, pointing a gun at someone is an assault), but the word is often loosely used to include both threatening acts and physical violence (see BATTERY).
Words alone cannot constitute an assault. Assault is a form of *trespass to the person and a crime as well as a tort: an ordinary (or common) assault, as described above, is a *summary offence punishable by a *fine at level 5 on the standard scale and/or up to six months’ imprisonment. Certain kinds of more serious assault are known as aggravated assaults and carry stricter penalties. Examples of these are assault with intent to resist lawful arrest (two years), assault occasioning *actual bodily harm (five years), and assault with intent to rob (life imprisonment).
The intentional or reckless application of physical force to someone without his consent. Battery is a form of *trespass to the person and is a *summary offence (punishable with a *fine at level 5 on the standard scale and/or six months’ imprisonment) as well as a tort, even if no actual harm results. If actual harm does result, however, the *consent of the victim may not prevent the act from being criminal, except when the injury is inflicted in the course of properly conducted sports or games (e.g.rugby or boxing) or as a result of reasonable surgical intervention.
Duty of care,
The legal obligation to take reasonable care to avoid causing damage.
There is no liability in tort for *negligence unless the act or omission that causes damage is a breach of a duty of care owed to the claimant. There is a duty to take care in most situations in which one can reasonably foresee that one’s actions may cause physical damage to the person or property of others. The duty is owed to those people likely to be affected by the conduct in question. Thus doctors have a duty of care to their patients and users of the highway have a duty of care to all other road users. But there is no general duty to prevent other persons causing damage or to rescue persons or property in danger, liability for careless words is more limited than liability for careless acts, and there is no general duty not to cause economic loss or psychiatric illness. In these and some other situations, the existence and scope of the duty of care depends on all the circumstances of the relationship between the parties. Most duties of care are the result of judicial decisions, but some are contained in statutes, such as the Occupiers’ Liability Act 1957
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Negligence and Carelessness amounting to the culpable breach of a duty: failure negligent misstatement 328 329 NHS Trust to do something that a reasonable man (i.e. an average responsible citizen) would do, or doing something that a reasonable man would not do. In cases of professional negligence, involving someone with a special skill, that person is expected to show the skill of an average member of his profession. Negligence may be an element in a few crimes, e.g. *careless and inconsiderate driving, and various regulatory offences, which are usually punished by fine. The main example of a serious crime that may be committed by negligence is *manslaughter (in one of its forms). When negligence is a basis of criminal liability, it is no defence to show that one was doing one’s best if one’s conduct still falls below that of the reasonable man in the circumstances. See also GROSS NEGLIGENCE. 2. A tort consisting of the breach of a *duty of care resulting in damage to the claimant. Negligence in the sense of carelessness does not give rise to civil liability unless the defendant’s failure to conform to the standards of the reasonable man was a breach of a duty of care owed to the claimant, which has caused damage to him. Negligence can be used to bring a civil action when there is no contract under which proceedings can be brought. Normally it is easier to sue for *breach of contract, but this is only possible when a contract exists. Generally, fewer heads of damage can be claimed in negligence than in breach of contract, but the rules limiting the time within which actions can be brought (see LIMITATION OF ACTIONS) may be more advantageous for actions in tort for negligence than for actions in contract. See also CONTRIBUTORY NEGLIGENCE; RES IPSA LOQUITUR.
Legal liability imposed on one person for torts or crimes committed by another (usually an employee but vicarious performance 526 527 violent disorder sometimes an *independent contractor or agent), although the person made vicariously liable is not personally at fault. An employer is vicariously liable for torts committed by his employees when he has authorized or ratified them or when the tort was committed in the course of the employees’ work. Thus negligent driving by someone employed as a driver is a tort committed in the course of his employment, but if the driver were to assault a passing pedestrian for motives of private revenge, the assault would not be connected with his job and his employer would not be liable. The purpose of the doctrine of vicarious liability is to ensure that an employer pays the costs of damage caused by his business operations. His vicarious liability, however, is in addition to the liability of the employee, who remains personally liable for his own torts. The person injured by the tort may sue either or both of them, but will generally prefer to sue the employer.
Vicarious criminal liability may effectively be imposed by statute on an employer for certain offences committed by an employee in relation to his employment. Thus it has been held that an employer is guilty of selling unfit food under the Food Act 1984 when his employee does the physical act of selling (the employee is also guilty, though in practice is rarely prosecuted). Likewise, an employer may be guilty of supplying goods under a false trade description when it is his employee who actually delivers them. For an offence that normally requires mens rea,an employer will only be vicariously liable if the offence relates to licensing laws. For example, if a licensee has delegated the entire management of his licensed premises to another j:letson, and that j:letson has committed the offence with the nec~ssatymens YeQ, th~ licensee will be vicariously liable.
Vicarious liability for crimes may be imposed in certain other circumstances. The registered owner of a vehicle, for example, is expressly made liable by statute for fixed-penalty and excess parking charges, even if the fault for the offence was not his. If the offence is a regulatory offence of *strict liability, the courts often also impose vicarious liability if the offence is defined in the statute in a way that makes this possible.
Scope of practice (the legal and professional boundaries imposed upon you as a nurse)
Advocacy (the nurse’s role as an advocate for the client)
An officer of the Crown whose principal function is to investigate deaths suspected of being violent or unnatural. He will do this either by ordering an *autopsy or conducting an *inquest. The coroner also holds inquests on *treasure trove. Coroners are appointed by the Crown from among barristers, solicitors, and qualified medical practitioners of not less than five years’ standing.
Colour. The normal colour of urine is pale straw or light yellow.Â It is mainly due to the pigment urochrome and partly to urobilin.Â Women’s urine is slightly lighter.Â If the quantity of urine is increased or there is a diminution or dilution of urinary pigments, it becomes lighter and rendered very pale as in excessive drinking, nervousness, anaemia, chlorosis, diabetes, hysteria, epilepsy, poluria, in general debility and in chronic interstitial nephritis. The colour of the urine will depend on the degree of concentration; the more concentrated-the darker; the greater the quantity of water -the lighter.Â Acid urine is slightly darker than alkaline urine. Urine becomes deeper in colour, like orange or dark yellow or brownish red generally known as high coloured or concentrated urine and is due to uroerythrin and urobilin produced by increased haemolysis, as in. fevers, after journeys, in hot days, in nervous excitability and after bodily exercises. Normal urine on standing for a time will have a white or sometimes a bluish white scum on the surface due to contamination and putrefaction.Â Urine glairy, whitish in colour indicates admixture with pus or leucorrhceal discharges. Urine coloured smoky, brown, reddish, brownish black or black indicates admixture with blood and denotes haemorrhage. Urine coloured greenish yellow or greenish brown indicates admixture with bile and denotes jaundice and other affections of the liver. Urine coloured milky indicates admixture with fat or pus and denotes chyluria or any purulent disease of the genitourinary tract.Â Urine coloured blue indicates typhus fever, admixture with methylene blue or when there is excess of indigogens. Many drugs after absorption colour the urine, such as yellowish orange by santonin and chrysophanic acid; reddish or orange brown by senna and rhubarb; dark olive green or black by carbolic acid and other coaltar derivatives while antipyrin reddens the urine.
Odour.Â When just voided urine is faintly aromatic but after a few minutes its characteristic odour is “urinous.”Â The odour of urine is due to phenol.Â It becomes pungent in concentrated urine, when urea is liberated in excess.Â It becomes ammoniacal and putrescent and the reaction becomes alkaline after sometime when this excess of urea takes up water and is converted into ammonium carbonate.Â It occurs quickly in urine from chronic cystitis or from suppurating diseases of kidney and bladder i.e., when urine is mixed with pus; blood or excessive phosphates.Â The odour of urine in diabetes and in acetonuria is slightly sweetish.Â The characteristic odour of garlic, sandal oil, cubebs, copaiba are given off when they are taken internally.Â Turpentine gives an odour of violets.
Appearance, physical character or transparency is the naked eye appearance of urine. Normal urine is always clear when voided but when allowed to stand for sometime it becomes slightly hazy or turbid due to suspended particles or from a slight cloud of mucus and epithelium. After sometime there may be sediments at the bottom due to gravity. If the urine is ammoniacal or decomposed a white turbidity forms due to sedimentation of phosphates or from bacterial activity. The turbidity or sediment is due mainly to the following suspended particles:-
- Uric Acid.
To distinguish one from another, first of all fill three fourths of a test tube with urine and very gently heat the upper portion of the urine, holding the test tube by the bottom.Â Now note whether the urine becomes clear or a cloudiness appears in the boiled portion, comparing with the lower unboiled portion of the test tube.Â If the urine is turbid and clears up on heating then it contains Urates.Â If the urine is clear and becomes cloudy with heat, before boiling point, then it is Albumen.Â If the urine is clear and becomes cloudy at the boiling point, then it is Phosphate.Â To distinguish between albumin and phosphate add 3 or 4 drops of acetic acid on the cloudy urine.Â If the cloudiness disappears, then it is phosphate; but if the cloudiness remains or thickens, then it is albumin.Â Lastly to distinguish between albumin and mucin add 2 drops of nitric acid, if the cloudiness disappears, then it is Mucin, but if the cloudiness still persists, it is albumin. The turbidity of carbonates will clear up with effervescence on addition of nitric acid whereas heat and acid increases the turbidity due to albumin.
To distinguish between phosphate and oxalate take some fresh urine and add ammonia, when there will be a precipitate. If on the addition of a few drops of acetic acid, the precipitates disappear, then it is phosphate, if it remains it is Oxalate. Failing the heat test take some urine in a test tube, preferably from the bottom and add a few drops of Liquor Potassae. Mix it thoroughly and if it clears up, then it is mucus; but if it becomes gelatinous or ropy, it is Pus.
Next, if the deposit is coloured then take some urine in a test tube, preferably from the bottom and add a few drops of caustic potash and gently heat a little.Â If it is dissolved, then it is Uric acid but if there is a precipitate, note the colour of the coagulum; if it is reddish brown or bottle green, it is Blood.
If the urine is turbid and there is no change either by heat or by addition of caustic potash and heat, then the turbidity is due to Micro-organisms.Â They generally clear up on the addition, of watery solution of ferric chloride and ammonium hydrate and then filter the urine.Â Sometime the character, colour and reaction will roughly denote the element.
Urates-They look like moss and are yellowish white or pink in colour.Â Reaction is generally acid. They deposit when the urine becomes cold.
Uric Acid-It is crystalline and reddish brown in colour, resembling a shower of ”cayenne pepper grains.” Reaction is moderately acid.
Phosphate-It forms a thin deposit and is white or yellowish white in colour.Â Reaction may be slightly acid, alkaline or neutral.
Mucus-It is a cloudy or woolly looking white deposit. Reaction is slightly acid.
Oxalate-It is soft, shining and white in colour. Reaction is generally slightly acid.
Pus- It looks like a ropy or creamy deposit, and is white in colour.Â Reaction is slightly acid or alkaline.
Blood-It is clotted or thready and is red smoky or brownish in colour.Â Reaction generally alkaline or may be slightly acid.
Micro-organisms-The deposit is slightly hazy and white in colour.Â They generally stick to the sides of the glass.
COMPLICATIONS OF FRACTURES
The majority of fractures heal without complications. If death occurs after a fracture, it is usually the result of damage to underlying organs and vascular structures or from complications of the fracture or immobility. Complications of fractures may be either direct or indirect. Direct complications include problems with bone infection, bone union, and avascular necrosis. Indirect complications are associated with blood vessel and nerve damage resulting in conditions such as compartment syndrome, venous thromboembolism, fat embolism, rhabdomyolysis (breakdown of skeletal muscle), and hypovolemic shock. Although most musculoskeletal injuries are not life threatening, open fractures, fractures accompanied by severe blood loss, and fractures that damage vital organs (e.g., lung, heart) are medical emergencies requiring immediate attention.
Compartment syndrome is a condition in which swelling and increased pressure within a limited space (a compartment) press on and compromise the function of blood vessels, nerves, and/or tendons that run through that compartment. Compartment syndrome causes capillary perfusion to be reduced below a level necessary for tissue viability. Compartment syndrome usually involves the leg, but can also occur in the arm, shoulder, and buttock.
Thirty-eight compartments are located in the upper and lower extremities. Two basic causes of compartment syndrome are (1) decreased compartment size resulting from restrictive dressings, splints, casts, excessive traction, or premature closure of fascia; and (2) increased compartment contents related to bleeding, inflammation, oedema, or IV infiltration.
Oedema can create sufficient pressure to obstruct circulation and cause venous occlusion, which further increases oedema. Eventually arterial flow is compromised, resulting in ischemia to the extremity. As ischemia continues, muscle and nerve cells are destroyed over time, and fibrotic tissue replaces healthy tissue. Contracture, disability, and loss of function can occur. Delays in diagnosis and treatment cause irreversible muscle and nerve ischemia, resulting in a functionally useless or severely impaired extremity.
Compartment syndrome is usually associated with trauma, fractures (especially the long bones), extensive soft tissue damage, and crush injury. Fractures of the distal humerus and proximal tibia are the most common fractures associated with compartment syndrome. Compartment injury can also occur after knee or leg surgery. Prolonged pressure on a muscle compartment may result when someone is trapped under a heavy object or a person’s limb is trapped beneath the body because of an obtunded state such as drug or alcohol overdose.
Compartment syndrome may occur initially from the body’s physiologic response to the injury, or it may be delayed for several days after the original insult or injury. Ischemia can occur within 4 to 8 hours after the onset of compartment syndrome.
One or more of the following six Ps are characteristic of compartment syndrome: (1) pain distal to the injury that is not relieved by opioid analgesics and pain on passive stretch of muscle traveling through the compartment; (2) increasing pressure in the compartment; (3) paraesthesia (numbness and tingling); (4) pallor, coolness, and loss of normal colour of the extremity; (5) paralysis or loss of function; and (6) pulselessness, or diminished or absent peripheral pulses.
Prompt, accurate diagnosis of compartment syndrome is critical.17 Perform and document regular neurovascular assessments on all patients with fractures, especially those with an injury of the distal humerus or proximal tibia or soft tissue injuries in these areas. Early recognition and effective treatment of compartment syndrome are essential to avoid permanent damage to muscles and nerves.
Carefully assess the location, quality, and intensity of the pain (see Chapter 9). Evaluate the patient’s level of pain on a scale of 0 to 10. Pain unrelieved by drugs and out of proportion to the level of injury is one of the first indications of impending compartment syndrome. Pulselessness and paralysis (in particular) are later signs of compartment syndrome. Notify the health care provider immediately of a patient’s changing condition.
Because of the possibility of muscle damage, assess urine output. Myoglobin released from damaged muscle cells precipitates and causes obstruction in renal tubules. This condition results in acute tubular necrosis and acute kidney injury.Â Common signs are dark reddish brown urine and clinical manifestations associated with acute kidney injury (see Chapter 47).
Elevation of the extremity may lower venous pressure and slow arterial perfusion. Therefore the extremity should not be elevated above heart level. Similarly, the application of cold compresses may result in vasoconstriction and exacerbate compartment syndrome. It may also be necessary to remove or loosen the bandage and split the cast in half (bivalving). A reduction in traction weight may also decrease external circumferential pressures.
Surgical decompression (e.g., fasciotomy) of the involved compartment may be necessary (Fig. 63-15). The fasciotomy site is left open for several days to ensure adequate soft tissue decompression. Infection resulting from delayed wound closure is a potential problem after a fasciotomy. In severe cases of compartment syndrome, an amputation may be required.
Compartment syndrome is a condition that occurs when elevated pressure within a limited space compromises the circulation, with increased risk of irreversible damage to its contents and their function. Acute compartment syndrome is a surgical emergency.
958.90 Compartment syndrome unspecified
958.90 Compartment syndrome, not otherwise specified
T79.A0 Compartment syndrome, unspecified, initial encounter
M79.A11 Nontraumatic compartment syndrome of right upper extremity
M79.A12 Nontraumatic compartment syndrome of left upper extremity
M79.A19 Nontraumatic compartment syndrome of unspecified upper extremity
M79.A21 Nontraumatic compartment syndrome of right lower extremity
M79.A22 Nontraumatic compartment syndrome of left lower extremity
M79.A29 Nontraumatic compartment syndrome of unspecified lower extremity
M79.A9 Nontraumatic compartment syndrome of other sites
T79.A19A Traumatic compartment syndrome of unspecified upper extremity, initial encounter
T79.A21A Traumatic compartment syndrome of right lower extremity, initial encounter
T79.A22A Traumatic compartment syndrome of left lower extremity, initial encounter
T79.A29A Traumatic compartment syndrome of unspecified lower extremity, initial encounter
EPIDEMIOLOGY & DEMOGRAPHICS
- Occurs most commonly after acute trauma, especially with long bone fractures, comprising 75% of cases.
- It usually occurs in persons <35 yr.
- Incidence is higher in males.
- It can occur in other parts, such as the foot, thigh, gluteal region, and abdomen.
- Supracondylar fractures in children can commonly lead to compartment syndrome.
- 6% to 9% of open tibial fractures are complicated by compartment syndrome.
- It is seen in all races and ethnicities.
Compartment syndrome occurs when the blood flow is less than the tissue metabolic demands, causing tissue injury. It occurs when the intracompartmental pressure increases limiting venous outflow with rising venous pressure, resulting in compromise of the local circulation and tissue hypoxia with decreased arteriovenous pressure gradient. Venous congestion additionally leads to tissue edema and interstitial pressure, and the compartment pressure continues to increase. Compartment pressure ranges between 10 and 30 mm Hg of diastolic pressure are able to cause the condition.
Different conditions are known to cause compartment syndrome:
- Conditions that limit compartment volume, such as when patients have fracture casts, when sedated or comatose patients lie on a limb for a prolonged period, or when patients have tight dressings that are applied externally.
- Conditions that cause increased compartment content, such as bleeding in the compartment from vascular injury or diathesis, fractures or finger injuries, reperfusion after ischemic injury such as embolectomy and arterial bypass grafting, severe bruising of muscle, and thermal or electrical burn injuries.
- Other injuries, such as extravasation of intravenous fluids, injection of recreational drugs, and snake bites.
PHYSICAL FINDINGS & CLINICAL
Signs and symptoms are usually apparent but can be unreliable and can lead to delayed diagnosis. Acute compartment syndrome can worsen within hours; therefore serial examination is important in a patient with suspected compartment syndrome. Patients with tense painful limbs are considered to have acute compartment syndrome; however, diagnosis is confirmed with the assessment of elevated compartment pressure. Clinical signs and symptoms include the following:
- Pain disproportional to injury (the earliest sign)
- Constant deep pain and pain that is referred to the compartment on passive stretching of the muscles of the affected compartment
(Fig. E1C-84, A)
- Reduced sense of touch or sensation (hypesthesia) within the territory of the nerve passing the compartment (in acute anterior compartment syndrome, the patient may have hypesthesia in the territory of the first webspace)
- Tense and swollen compartment (Figs. E1C- 84, B and 1C-84, C)
- Muscle weakness
- Paresis (late finding) that suggests permanent muscle damage
- Capillary refill can be slow but normal.
- Peripheral pulses that are normally palpable even in severe conditions
- Tingling and numbness in the affected limb. Hypesthesia or paresthesia should be evaluated with pinprick, light touch, and two-point discrimination tests.
- Difficulty moving the extremities.
Diagnosis is based on clinical signs and symptoms along with compartment pressure.
Compartment pressure testing may be unnecessary if the diagnosis is clinically obvious.
- Muscle strains
- Peripheral vascular injury
- Necrotizing fasciitis
- Stress fractures
- Deep vein thrombosis and thrombophlebitis
- Muscle contusion
- Tarsal tunnel syndrome
- Posterior ankle syndrome
- Popliteal artery impingement
- Venous insufficiency
Diagnosis is based on clinical findings and the measurement of compartment pressures.
Laboratory values are not useful in the diagnosis of compartment syndrome but are important for other diagnoses or associated conditions.
- CBC with differential for evaluation of infection
- Creatine phosphokinase (CK) levels, which can rise as muscle injury develops
- Metabolic panel for the assessment of electrolytes and renal function
- Coagulation profile for bleeding diathesis
- Urinalysis for rhabdomyolysis
- Urine and serum myoglobin levels
FIGURE 1C-84 C: A, Severe calf swelling due to anterior and posterior compartment syndromes after ischemia-reperfusion. B, Appearance after emergency fasciotomy. Note edematous muscle and hematoma. (Courtesy Michael J. Allen, FRCS, Leicester, UK. From Floege J et al: Comprehensive clinical nephrology, ed 4, Philadelphia, 2010, Saunders.)
Compartment Syndrome 307
Diseases and Disorders
- Direct intracompartmental pressure measurement can be done by handheld manometer, wick or slit catheter technique, and simple needle manometer system. Compartment syndrome is diagnosed when the difference between diastolic blood pressure and compartment pressure (Î” pressure) is â‰¤30 mm Hg.
- Ultrasonography can be used to rule out deep vein thrombosis, or Doppler ultrasonography can be used to evaluate blood flow to the extremity. Arteriography should be used to evaluate the adequate blood flow through a compartment.
- Near-infrared spectroscopy and technetium- 99m methoxyisobutylisonitrile scintigraphy can also be used.
- Radiography can be used on the affected limb for fracture or foreign body evaluation.
Treatment goal is to keep intracompartmental pressure low and prevent tissue injury (Fig. 1C-84, D).
- Immediate relieving of all external pressure on the affected compartment
- Removal of casts, splints, and dressings
- Placing limb at heart level to avoid decreased or increased blood flow
ACUTE GENERAL Rx
- Analgesics for pain
- Hyperbaric oxygen
- Hypotension can worsen tissue ischemia and thus should be treated with IV isotonic saline.
- Fasciotomy of the affected compartment is indicated if there has been >6 hr of limb ischemia, or immediate decompression should be performed when the compartment pressure > 30 to 35 mm Hg.
- Measurement of compartment pressure is not necessary to perform fasciotomy if clinical suspicion is high depending on history and clinical examination.
- When compartment pressures are trending downward, it is often safe to delay emergent fasciotomy, provided the Î” pressure is also improving.
- Aftercare of fasciotomy wound: Wound is inspected after 48 hours and dead tissue is removed.
- Wounds are left open, requiring later skin grafting or delayed wound closure.
- Opsite sheet and boot lace techniques are also used for closing fasciotomy wounds.
- Concomitant fractured bones should also be stabilized with plating, external fixation, or intramedullary nailing.
With early diagnosis and treatment, the prognosis is excellent for recovery of the muscles and nerves inside the compartment. The following conditions can be prevented:
- Permanent nerve damage/paralysis
- Muscle contracture
- Muscle necrosis
- Fracture nonunion
- Rhabdomyolysis that leads to renal failure
- Compartment syndrome that can occur in open fractures
- Permanent nerve injury, which can occur after 12 to 24 hr of compression; mortality rates in patients who need fasciotomy is â‰ˆ15%.
Patients with suspected compartment syndrome should be referred promptly to orthopedic and general surgery.
PEARLS & CONSIDERATIONS
- Universal precautions and aseptic measures are necessary for patients undergoing fasciotomy because the risk of local and systemic infection is high with the procedure.
- Invasive monitoring techniques should be undertaken with adequate analgesia so that patient immobility is ensured while the pressure is measured.
- Injection of local anaesthetics into the compartment can increase the pressure and pain and therefore should be avoided.
- Patients with fracture casts should be informed about the risks of swelling, and patients should also be encouraged to wear appropriate equipment while playing sports.
- A history of coagulation disorders and the use of anticoagulants should be mentioned in a patient’s medical history.
Assault has two different interpretations.
1. Traditionally called common assault and consisting of the making of an unlawful and intentional (or possibly only reckless) threat to inflict imminent force against the person where the victim was aware of the threat.Â A distinction was previously maintained at common law between common assault and battery.Â Increasing codification of criminal law has resulted in abandonment of this distinction and in Australia ‘assault’ now commonly refers both to common assault and actual infliction of force.Â Statutory provisions for the different states are numerous and terminology varies (e.g. offences of ‘causing injury’ or ‘threatening’).
2. One of three ma
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